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MultiCaRe_Reasoning96400 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 76.0
Sex: Male
Title: Utility of F-18 FDG PET/CT for Detection of Bone Marrow Metastases in Prostate Cancer Patients Treated with Radium-223
Keywords: bone marrow; pet; prostate cancer; radiotherapy; radium;
Abstract:
A 76-year-old man with symptomatic bone metastases from castration-resistant prostate cancer underwent Radium-223-dichloride (Ra-223) therapy. Before Ra-223 therapy, he had normal peripheral blood cell counts. Ra-223 therapy relieved his shoulder and low back pain. The elevation of the serum prostate-specific antigen (PSA), doubling every month during Ra-223 therapy, suggested a PSA flare or relapse. Some lesions showed decrease and some lesions showed increase on Tc-99m hydroxymethylene diphosphonate bone scintigraphy at two weeks after the third injection of Ra-223 therapy. Ra-223 therapy was discontinued due to thrombocytopenia that was getting worse rapidly. After treatment discontinuation, namely four weeks after the third injection of Ra-223, F-18 fluorodeoxyglucose (FDG) Positron Emission Tomography (PET)/CT and a biopsy were performed to evaluate for metastases, and bone marrow metastases were found. Ra-223 was effective for osteoblastic lesions, but not for bone marrow metastases. FDG PET/CT, but not a Tc-99m based bone scan, detected diffuse bone marrow involvement by cancer. This case report is the first to clarify the utility of FDG PET for the detection of bone marrow metastases confirmed by pathological examination in Ra-223 therapy for progressive castration-resistant prostate cancer.
Image Caption and Description:
Image caption: Peripheral blood cell counts before, during, and after Ra-223 treatment. White and red blood cell (WBC, RBC, respectively) and platelet (PLT) counts are normal before and decreased during and after Ra-223 therapy. The patient has thrombocytopenia (with PLT of 11.9x104/muL at the third injection of Ra-223 therapy) and anemia (with a hemoglobin of 9.9 g/dL four weeks after the third injection of Ra-223 therapy), which rapidly gets worse. He became transfusion-dependent, presenting with a hemoglobin of 7.7 g/dL and requiring monthly red-cell transfusions.
Image description: Before Ra-223 therapy, his hemoglobin was 14.9 g/dL, with a leukocyte count of 5900/muL and a platelet count of 24x104/muL; all were normal (Figure 1).
Ra-223 therapy. PSA elevation suggested a PSA flare or relapse. Ra-223 therapy was discontinued due to thrombocytopenia (Figure 1).
Image caption: Prostate-specific antigen (PSA) and serum total alkaline phosphatase (ALP, marker indicating osteoblastic activity) trends and the response to Ra-223, with concomitant use of hormonal therapy. The PSA level is 64 ng/ml before Ra-223 therapy, and it increases by twice a month, with PSA peaking at 1303 ng/ml eight weeks after the third injection of Ra-223 therapy. ALP decreases from 506 to 361 U/L during Ra-223 therapy, compatible with a favorable response to radiotherapy and concordant with the general decrease of Tc-99m HMDP uptake in bone lesions.
Image description: He had remained on androgen deprivation therapy with a novel endocrine agent, first enzalutamide and then abiraterone, with Ra-223 therapy (Figure 2).
Image caption: Tc-99m HMDP bone scintigraphy: images from left to right, pretreatment (posterior and anterior views) and 2 weeks after the third injection (posterior and anterior views) of Ra-223 therapy. Ra-223 therapy has somewhat reduced abnormal uptake on right shoulder and lumbar vertebra with pain relief, and somewhat increased uptake on some parts of skull, left jaw, sternum, thoracic vertebra, and patchy and mixed of increased and decreased uptake on humeri and femur in bone metastases. Meanwhile, the serum PSA level increases from 64 ng/mL before treatment to 869 ng/mL at 4 weeks after the third injection of Ra-223 therapy.
Image description: Tc-99m HMDP bone scintigraphy (Figure 3). To evaluate for metastases, FDG PET/CT was performed four weeks after the third injection of Ra-223 therapy and showed diffuse FDG uptake in bone without osteoblastic lesions (Figure 4).
Image caption: F-18 FDG PET maximum intensity projection (MIP) image (A), axial pelvic PET (B), CT (C), and fused PET/CT (D) at 4 weeks after the third injection of Ra-223 therapy. Diffuse FDG uptake in the bone without osteoblastic lesions shows active osteolytic metastases or bone marrow involvement. Osteoblastic lesions without FDG correspond to lesions with decreased HMDP uptake.
Image description: Tc-99m HMDP bone scintigraphy (Figure 3). To evaluate for metastases, FDG PET/CT was performed four weeks after the third injection of Ra-223 therapy and showed diffuse FDG uptake in bone without osteoblastic lesions (Figure 4).
Image caption: The images of a bone marrow biopsy are shown. Hematoxylin and eosin stain (A), x400. Histologically, small round cells are diffusely spread in bone marrow. There is no ordinary tubular formation, as shown in adenocarcinoma of the prostate. On immunostaining, x400, androgen receptor (B) and cytokeratin AE1/3 (C) are both positive. Strong androgen receptor nuclear staining (B) indicates histological malignancy. Positive immunostaining for prostate-specific antigen is confirmed in some cells (D), which is not inconsistent with low-grade prostatic carcinoma. The microscopic examination shows bone marrow infiltration with prostate carcinoma.
Image description: Bone marrow metastasis was confirmed by pathological examination following FDG PET/CT-guided bone marrow biopsy (Figure 5).
Case Report:
A 76-year-old man with symptomatic bone metastases from hormone-refractory prostate cancer underwent Ra-223 therapy (3 of the planned 6 intravenous injections at a dose of 55 kBq per kg body weight, every 4 weeks). Before Ra-223 therapy, his hemoglobin was 14.9 g/dL, with a leukocyte count of 5900/muL and a platelet count of 24x104/muL; all were normal (Figure 1). The serum testosterone level was 0.26 ng/ml. Abdominal pelvic CT was performed to document the presence of unequivocal visceral metastases before Ra-223 therapy.
He had remained on androgen deprivation therapy with a novel endocrine agent, first enzalutamide and then abiraterone, with Ra-223 therapy (Figure 2). A decreased serum total alkaline phosphatase (ALP), PSA elevation (Figure 2) and blood cell count decreases (Figure 1) continued during Ra-223 therapy. PSA elevation suggested a PSA flare or relapse. Ra-223 therapy was discontinued due to thrombocytopenia (Figure 1). After the third injection of Ra-223, images showed that the decreased uptake in some parts corresponding to the pain relief lesion, and the increased uptake in some parts without pain on Tc-99m HMDP bone scintigraphy (Figure 3). To evaluate for metastases, FDG PET/CT was performed four weeks after the third injection of Ra-223 therapy and showed diffuse FDG uptake in bone without osteoblastic lesions (Figure 4). Bone marrow metastasis was confirmed by pathological examination following FDG PET/CT-guided bone marrow biopsy (Figure 5). He had received neither chemotherapy nor granulocyte-colony stimulating factor therapy that could have caused diffuse bone marrow FDG uptake.
OUTPUT:
| PMC5765335 |
MultiCaRe_Reasoning96401 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 26.0
Sex: Female
Title: Cutaneous tube ureterostomy: a fast and effective method of urinary diversion in emergency situations
Keywords: ureter; trauma; tube cutenuous ureterostomy;
Abstract:
Aim:
To report on a simple and rapid method of urinary diversion. This method was applied successfully in different clinical scenarios when primary reconstruction of the ureters was not possible.
Materials and methods:
The disconnected ureter is catheterized by a feeding tube. The tube is secured with sutures and brought out to the lateral abdominal wall as cutaneous tube ureterostomy (CTU).
Results:
This method was applied in three different clinical scenarios: a 40-year-old man who sustained multiple high-velocity gunshots to the pelvis with combined rectal and bladder trigone injuries and massive bleeding from a comminuted pubic fracture. Damage control included colostomy and bilateral CTUs. A 26-year-old woman had transection of the right lower ureter during abdominal hysterectomy. Diagnosis was delayed for 3 weeks when the patient developed sepsis. The right kidney was diverted with a CTU. A 37-year-old male suffered from bladder perforation and hemorrhagic shock. Emergency cystectomy was done and urinary diversion was accomplished with bilateral CTUs. In all cases, effective drainage of the urinary system was achieved with normalization of kidney function.
Conclusion:
When local or systemic conditions preclude definitive repair and damage control surgery is needed, CTU provides fast and effective urinary diversion.
Image Caption and Description:
Image caption: Photos of Case 1.. Notes: (A) Intra-operative view showing a large midline urinoma. (B) Isolation of the ureter above the hematoma. (C) Intubation of the ureter with a 10 Fr feeding tube. (D) Nephrostogram done after the definitive surgery demonstrating passage of contrast from the kidney to the ureter and then to the bladder through an ileal segment (a mosaic of three fluoroscopy fields).
Image description: Midline laparotomy revealed a large urinoma in the midline (Figure 1A).
The ureter was dissected higher until a normal ureter was found (Figure 1B).
A 10 Fr feeding tube was placed in the right ureter and secured with polydioxanone 2/0 sutures (Figure 1C).
Three months later an ileal interposition was performed uneventfully (Figure 1D).
Case Report:
Case 1 : a 26-year-old previously healthy woman, a mother of seven children, was transferred from another hospital in a state of septic shock. Three weeks earlier, the patient developed massive postpartum hemorrhage following spontaneous vaginal delivery and emergent total abdominal hysterectomy was done. Postoperatively, the patient developed severe lower abdominal and right flank pain, chills, and vomiting and was transferred to our institution. Physical examination disclosed a hemodynamically stable patient with temperature of 38.90 C and a lower abdominal tender mass which was palpable also on vaginal examination. Blood tests revealed white blood count of 23,000 per mm3 and hemoglobin level of 10.6 g/dL. Blood biochemistry including renal function tests were within normal limits. The patient was taken to the operating room by a gynecological team with a presumed diagnosis of Douglas pouch abscess, but puncture of the posterior fornix yielded urine. Urologic consultation was requested. Cystoscopy revealed normal urethra, bladder, and ureteral orifices. Retrograde urethrography showed normal left ureter and collecting system and complete transection of the right ureter 5 cm above the bladder level. Cystogram was normal. Midline laparotomy revealed a large urinoma in the midline (Figure 1A). The small bowel was edematous and covered with fibrin. In addition, several large hematomas surrounding the right ureter, which was draining urine freely, were noticed. Due to the septic condition of the patient and the presence of severely inflamed small bowel, it was decided not to perform a definitive repair. The ureter was dissected higher until a normal ureter was found (Figure 1B). A 10 Fr feeding tube was placed in the right ureter and secured with polydioxanone 2/0 sutures (Figure 1C). The distal end of the tube was brought out to the lateral abdominal wall as CTU. The postoperative course was uneventful. White blood count normalized the next day and the patient resumed normal diet on the second postoperative day. On the eighth postoperative day, a right nephrostomy tube was placed, the tube ureterostomy was closed on the skin and the patient discharged home. Three months later an ileal interposition was performed uneventfully (Figure 1D).
OUTPUT:
| PMC4468998 |
MultiCaRe_Reasoning96402 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 40.0
Sex: Male
Title: Cutaneous tube ureterostomy: a fast and effective method of urinary diversion in emergency situations
Keywords: ureter; trauma; tube cutenuous ureterostomy;
Abstract:
Aim:
To report on a simple and rapid method of urinary diversion. This method was applied successfully in different clinical scenarios when primary reconstruction of the ureters was not possible.
Materials and methods:
The disconnected ureter is catheterized by a feeding tube. The tube is secured with sutures and brought out to the lateral abdominal wall as cutaneous tube ureterostomy (CTU).
Results:
This method was applied in three different clinical scenarios: a 40-year-old man who sustained multiple high-velocity gunshots to the pelvis with combined rectal and bladder trigone injuries and massive bleeding from a comminuted pubic fracture. Damage control included colostomy and bilateral CTUs. A 26-year-old woman had transection of the right lower ureter during abdominal hysterectomy. Diagnosis was delayed for 3 weeks when the patient developed sepsis. The right kidney was diverted with a CTU. A 37-year-old male suffered from bladder perforation and hemorrhagic shock. Emergency cystectomy was done and urinary diversion was accomplished with bilateral CTUs. In all cases, effective drainage of the urinary system was achieved with normalization of kidney function.
Conclusion:
When local or systemic conditions preclude definitive repair and damage control surgery is needed, CTU provides fast and effective urinary diversion.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
Case 2: a 40-year-old male sustained multiple gunshot wounds during a terrorist attack. Several entrance wounds were noticed in the buttock and a single exit wound above the pubic symphysis was seen. Upon admission, the patient was neurologically intact, but tachycardic. Rectal examination showed bloody discharge. After initial fluid resuscitation the patient was transferred to the operating room and a laparotomy performed. Combined rectal and urological injuries were evident including wide, bleeding tears of the rectum and bladder trigone. A comminuted pubic fracture was also evident. Shortly after opening the peritoneal cavity, the patient bled profusely from the pelvis and developed hemorrhagic shock despite massive transfusion. A "damage control" procedure was carried out. The rectum was closed with a stapler and end sigmoid diversion colostomy was constructed. The bladder was explored; the left ureteral orifice was identified and catheterized while the right one could not be identified. The bladder was closed rapidly with a single suture line. The ureters were identified and transected at the level of the common iliac vessels and brought out to the abdominal wall as tube ureterostomies. Temporary abdominal closure using a plastic bag was carried out. The postoperative course was remarkable for severe sepsis with multi-organ failure. Repeated open debridement of pelvic necrotic tissue and abscess drainage was performed. During this period urinary output through the ureterostomies was satisfactory with normal renal function. Three weeks after the injury the patient's condition stabilized. The tube ureterostomies were removed after the insertion of nephrostomies. Later, the abdomen was closed with skin graft and the patient discharged home with two opened nephrostomies and a well-functioning colostomy.
One year after the injury, evaluation revealed vesicorectal fistula, small bladder capacity (100 cc) with left vesicoureteral reflux to the point of the transection, normal anal and urethral sphincters and normal erection. Definitive surgery included division of the fistula, closure of colostomy, and anastomosis of the proximal colon to the lower rectum, left uretero-ureterostomy, augmentation ileocystoplasty, right ileal interposition, and protecting ileostomy. Postoperative course was unremarkable, and a year later the ileostomy was closed. Four years later, the patient is potent and fully continent.
OUTPUT:
| PMC4468998 |
MultiCaRe_Reasoning96403 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 37.0
Sex: Male
Title: Cutaneous tube ureterostomy: a fast and effective method of urinary diversion in emergency situations
Keywords: ureter; trauma; tube cutenuous ureterostomy;
Abstract:
Aim:
To report on a simple and rapid method of urinary diversion. This method was applied successfully in different clinical scenarios when primary reconstruction of the ureters was not possible.
Materials and methods:
The disconnected ureter is catheterized by a feeding tube. The tube is secured with sutures and brought out to the lateral abdominal wall as cutaneous tube ureterostomy (CTU).
Results:
This method was applied in three different clinical scenarios: a 40-year-old man who sustained multiple high-velocity gunshots to the pelvis with combined rectal and bladder trigone injuries and massive bleeding from a comminuted pubic fracture. Damage control included colostomy and bilateral CTUs. A 26-year-old woman had transection of the right lower ureter during abdominal hysterectomy. Diagnosis was delayed for 3 weeks when the patient developed sepsis. The right kidney was diverted with a CTU. A 37-year-old male suffered from bladder perforation and hemorrhagic shock. Emergency cystectomy was done and urinary diversion was accomplished with bilateral CTUs. In all cases, effective drainage of the urinary system was achieved with normalization of kidney function.
Conclusion:
When local or systemic conditions preclude definitive repair and damage control surgery is needed, CTU provides fast and effective urinary diversion.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
Case 3: a 37-year-old male with multiple sclerosis treated with high-dose steroids was admitted through the emergency department with urosepsis, urinary retention, and acute renal failure. The patient was hospitalized in the intensive care unit and a catheter was inserted. Two days after admission, the patient developed peritonitis and hemorrhagic shock. Computed tomography (CT) showed perforation of the bladder. Blood products and fluids were given and emergent laparotomy was done. Intra-peritoneal bladder tear was found and repaired in multiple layers. After surgery, bleeding continued and a cystogram showed a massive leak from the suture line. A second attempt to close the bladder was done 2 days after the first surgery. The patient's condition continued to be critical with blood product consumption and renal failure with creatinine level that reached 915 mmol/L. Another cystogram showed that the bladder was completely open. A third laparotomy was done 2 days after the second surgery. Massive bleeding from multiple points in the bladder was noticed. The ureteral orifices were catheterized with feeding tubes number 8 and cystectomy was done. The ureteral catheters were brought out of the abdominal wall as CTUs. The patient's hemodynamic condition stabilized, blood consumption ceased, and a high urinary output through the ureterostomies was recorded with a decrease in creatinine level to 133 mmol/L. On the third day after the third surgery focal face convulsion was noticed. CT showed diffuse brain edema. This was attributed to sepsis. The patient's general condition deteriorated and he died 7 days after the third operation. Pathological examination of the bladder showed atrophic detrusor muscle and an absence of the mucosal lining.
OUTPUT:
| PMC4468998 |
MultiCaRe_Reasoning96404 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 21.0
Sex: Male
Title: Fatal intoxication with N-ethylpentylone: a case report
Keywords: n-ethylpentylone; bath salts; cardiac arrest; cathinones; toxicology;
Abstract:
Synthetic cathinones represent the latest genre of new drugs of abuse, which are increasing in popularity in part because they are readily available and because they are not detected by routine drug testing. They provide a cheaper substitute to stimulants such as methamphetamine and cocaine and are sold on the internet and in retail establishments as 'bath salts,' 'plant food,' or 'research chemicals.' We report a case involving a 21-year-old male who suffered arrest-related death due to intoxication with N-ethylpentylone, a new cathinone derivative. He reportedly left his house to smoke marijuana and returned displaying extremely odd behavior. The patient was unresponsive upon presentation to the emergency room and was intubated after suffering cardiac arrest. Clinical laboratory values revealed elevated lactic acidosis, hyperkalemia, rhabdomyolysis, and renal injury. His condition continued to worsen despite medical management. Sudden cardiac arrest occurred again 72 hours into his hospital stay and the patient was pronounced dead. Post-mortem toxicology testing with gas chromatography and mass spectrometry determined the presence of N-ethylpentylone in the urine. This case report details the behavior effects, clinical presentation, and autopsy findings for N-ethylpentylone drug intoxication.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
A 21-year-old man left his house to reportedly smoke marijuana. When he returned, per his girlfriend, he was 'acting crazy.' Law enforcement was dispatched. He was described as combative, confused, and sweating heavily. Paramedics administered 5 mg of intramuscular haloperidol. He went into cardiac arrest shortly thereafter. Advanced cardiac life support protocol was initiated, and return of spontaneous circulation was achieved within 3 minutes. Upon arrival at the emergency room his blood pressure was 95/55 mmHg, heart rate 126 bpm, respiratory rate 25 bpm, and oxygen saturation 99% on 40% FiO2. On physical examination, he was noted to have multiple abrasions on his face, sluggish pupillary reflexes, negative vestibulo-occular reflex, and myoclonus at the right lower extremity. Initial electrocardiogram showed sinus rhythm with premature atrial complexes, ST depression in inferior leads, and corrected QT interval of 403 ms.
Clinical laboratory analysis revealed potassium 6.8 mmol/L, glucose 28 mg/dL, creatinine kinase 116,550 IU/L, lactic acid 28 mg/dL (without an osmolar gap), aspartate aminotransferase 12,374 IU/L, alanine aminotransferase 7,649 IU/L, and creatinine 1.70. Arterial blood gas showed severe metabolic acidosis with pH 6.80. Other laboratory values revealed elevated troponins and acute kidney injury. The patient was admitted to the intensive care unit and treated with hypothermia cooling measures, intravenous fluids, and bicarbonate.
Toxicology screening was positive only for cannabinoid and revealed an ethanol level of 12 mg/dL. Special testing for synthetic cannabinoid metabolites and 25I-NBOMe (5-HTA2 receptor agonist) was negative. Computed tomography of the head showed no abnormalities. However, magnetic resonance imaging of the brain showed bilateral restricted diffusion in the posterior parietal and occipital regions suggesting profound cerebral hypoxia. During the hospital course his lactic acidosis improved to 3.2 mmol/L with intravenous fluids, but his kidney function continued to worsen and creatinine kinase rose to 451,126 IU/L. On day 2, the patient was started on continuous renal replacement therapy due to oliguria and rising creatinine levels. Despite supportive treatment, he developed hypothermia with a temperature of 34.3 C, persistent hypocalcemia, and disseminated intravascular coagulation. On day 3, he developed severe hypotension requiring vasopressors for hemodynamic support. Approximately 72 hours after admission he went into cardiac arrest. Cardiopulmonary resuscitation was performed for 30 minutes and the patient was pronounced dead. Lab results during his hospitalization confirmed profound organ dysfunction and metabolic derangement in a previously healthy individual (Table 1).
An autopsy was performed at the Office of the Chief Medical Examiner in response to a concern about possible misconduct by law enforcement. Post-mortem toxicology testing using gas chromatography and mass spectrometry found N-ethylpentylone in the urine. The official cause of death was drug intoxication with N-ethylpentylone based on these autopsy findings, the clinical presentation, and the hospital course.
OUTPUT:
| PMC6197033 |
MultiCaRe_Reasoning96405 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 11.0
Sex: Female
Title: Multi-organ failure caused by lasagnas: A case report of Bacillus cereus food poisoning
Keywords: bacillus cereus; continuous venovenous hemofiltration; food poisoning; liver failure acute; pediatrics; sepsis;
Abstract:
We report a Bacillus cereus, cereulide producing strain, food poisoning of two sisters. After eating a few bites of pasta cooked 3 days earlier, a 13-year-old girl developed mild symptoms. However, her 11-year-old sister suffered, 40 h after ingestion of the entire platter, a multi-organ failure including acute liver failure, rhabdomyolysis, disseminated intravascular coagulation, and acute kidney injury (AKI). She received supportive care in pediatric intensive care using mechanical ventilation, hemofiltration, and high-doses vasopressors. She was specifically treated for toxin-mediated disease using blood purification and further digestive decontamination. This report highlights the potential severity of B. cereus food poisoning but also a successful dual treatment including toxin removal and antimicrobial treatment to prevent toxin production.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
A previously well 11-year-old girl was admitted to the pediatric emergency department for abdominal pain and emesis. She was with her family in a rental during an especially warm summer (40 C during the day). Symptoms started 20 min after she and her 13-year-old sister ate leftover lasagnas. Both sisters reported the meal was unusually smelly and had a bad taste of "old cheese," hence the elder stopped eating but not our patient. Both sisters presented abdominal pain and emesis and were brought to the hospital 6 h after the onset of symptoms. Parental interrogation reported the lasagnas had been prepared 72 h earlier and stored in a faulty refrigerator. They presented signs of clinical dehydration, had unremarkable laboratory results, and received intra-venous fluids. The 13-year-old girl's symptoms quickly improved, and she was discharged after 48 h of observation.
OUTPUT:
| PMC9516094 |
MultiCaRe_Reasoning96406 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 11.0
Sex: Female
Title: Multi-organ failure caused by lasagnas: A case report of Bacillus cereus food poisoning
Keywords: bacillus cereus; continuous venovenous hemofiltration; food poisoning; liver failure acute; pediatrics; sepsis;
Abstract:
We report a Bacillus cereus, cereulide producing strain, food poisoning of two sisters. After eating a few bites of pasta cooked 3 days earlier, a 13-year-old girl developed mild symptoms. However, her 11-year-old sister suffered, 40 h after ingestion of the entire platter, a multi-organ failure including acute liver failure, rhabdomyolysis, disseminated intravascular coagulation, and acute kidney injury (AKI). She received supportive care in pediatric intensive care using mechanical ventilation, hemofiltration, and high-doses vasopressors. She was specifically treated for toxin-mediated disease using blood purification and further digestive decontamination. This report highlights the potential severity of B. cereus food poisoning but also a successful dual treatment including toxin removal and antimicrobial treatment to prevent toxin production.
Image Caption and Description:
Image caption: Timeline of treatment for multi-organ failure.
Image description: She was started on sodium benzoate and sodium phenylbutyrate, n-acetylcysteine, and high-flow continuous veno-venous hemodiafiltration (Figure 1).
After 5 days of enteral vancomycin, stool cultures became negative (Figure 1), and the laboratory values improved.
Case Report:
Twenty-four hours after admission, our 11-year-old patient complained of chest pain and intense abdominal pain. On clinical examination, she was tachycardic and hypotensive and presented hematemesis. Her laboratory tests revealed a multi-organ involvement with acute kidney injury (AKI), acute liver failure, pancreatitis, rhabdomyolysis, and elevated cardiac enzymes (Table 1). She was referred to our pediatric intensive care unit (PICU) for hepatic transplantation.
On her arrival in PICU, she was drowsy [Glasgow coma scale (GCS) 13/15:Eye 3/4 Verbal 4/5 Motor 6/6], without respiratory nor hemodynamic failure. The rest of her physical examination was unremarkable, and her blood sugar levels were normal. Six hours after her admission, she suddenly became non-responsive (GCS 8/15) with clinical and trans-cranial Doppler pattern of cerebral edema and hepatic encephalopathy. She required oro-tracheal intubation, mechanical ventilation, osmotherapy, hypothermia, and aggressive hemodynamic support. Laboratory results confirmed hyperammonemia (230 mmol/L), rhabdomyolysis with anuric AKI (creatinine 218 mumol/L), and hyperkalemia (6.9 mmol/L). She was started on sodium benzoate and sodium phenylbutyrate, n-acetylcysteine, and high-flow continuous veno-venous hemodiafiltration (Figure 1). She was treated with extra-corporeal blood purification with an enhanced AN69 hemofilter with increased adsorption capacities of small molecules (oXiris, Baxter Acute Therapies). She was hypotensive and tachycardic despite 60 ml/kg of fluids boluses and high doses of norepinephrine (16 mg/h, i.e., 6.6 mug/kg/min). With this refractory vasoplegic shock, she was started on angiotensin 2 with a dose of 15 ng/kg/min and norepinephrine was gradually withdrawn and stopped on day 6 of ICU admission.
She was initially started on cefotaxime and micafungin according to the local acute liver failure guidelines. The acute liver failure etiological assessment including hepatotropic viruses, toxic, auto-immune hepatitis, Wilson's disease, and mitochondrial disorder was negative. On day 2 of ICU admission, the duty consultant suspected sepsis due to food-borne B. cereus toxin-mediated disease. The patient was started on IV vancomycin and benzylpenicillin. Emesis, stool, and blood were sent to the lab and confirmed the diagnosis. Bacillus cereus was cultured in stool and emesis. Toxins were evidenced in stool (cereulide and NHE toxins) and emesis (NHE toxin). The antibiogram of the bacteria was usual for B. cereus, with resistance to penicillin G and amoxicillin, intermediate resistance to piperacillin, and amoxicillin/clavulanate, and was sensitive to imipenem, gentamicin, macrolides, rifampicin, and cotrimoxazole. Despite 5 days of intravenous vancomycin, the patient had persistent B. cereus culture in stool samples and slow improvement of her laboratory in particular creatinine kinase and renal function, both partially masked by the previous use of renal replacement therapy. After discussion with the antimicrobial stewardship team, we changed the antibiotics to imipenem-cilastatin. However, as stool cultures showed numerous B. cereus colonies (Table 1) already at Day 5 and again at Day 11, and in view of a rebound in the rhabdomyolysis, we decided to add a 7-day treatment with enteral vancomycin for digestive decontamination. After 5 days of enteral vancomycin, stool cultures became negative (Figure 1), and the laboratory values improved.
Multi-organ dysfunction syndrome gradually regressed with complete neurological and hepatic recovery. The patient was on hemofiltration for 8 days, initially for AKI, blood purification, and hyperammonemia and after day 5 for AKI only. At PICU discharge, the renal function was persistently impaired (creatinine 124 mumol/L and urea 14.9 mmol/L) but did not require further hemodialysis or antihypertensive treatment. The patient was discharged to the ward on day 19 and home on day 40. Her neurological, renal, and hepatic status were normal upon discharge home and 24 months later.
OUTPUT:
| PMC9516094 |
MultiCaRe_Reasoning96407 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 70.0
Sex: Male
Title: Spinal cord ischemia after endovascular repair of infrarenal abdominal aortic aneurysm: a rare complication
Keywords: None
Abstract:
Neurologic deficit secondary to spinal cord ischemia after elective infrarenal, endovascular aneurysm repair (EVAR), consists a rare and rather disastrous complication. The etiology of such neurologic complication seems to be multifactorial, making this event unpredictable and foremost unpreventable. We report a case of paraparesis and bladder dysfunction that occurred immediately after the EVAR procedure. Prompt management by conservative or invasive methods seems to be important for the reversal of the neurologic deficit and the optimization of patient's outcome.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
A 70-year-old man with a history of coronary artery disease, chronic obstructive pulmonary disease, and hyperlipidemia was referred to our department for evaluation of a 5.5 cm AAA. The patient had previously undergone a 3 vessel coronary artery by-pass grafting and was under antiplatelet therapy with acetylsalicylic acid (320 mg/day). The anatomic configuration of the AAA fulfilled the requirements for EVAR. The infrarenal neck of the aneurysm was reverse-tapered, 12 mm in length, and 26 mm to 29 mm in diameter. Due to these anatomic characteristics, a graft with suprarenal fixation was selected. Under general anesthesia an endovascular bifurcated graft (Talent, Medtronic Vascular AVE, Medtronic Europe SA, Route du Molliau, Switzerland) of 32 mm in main body diameter, 16 mm in limb diameter, and 15.5 cm in length was implanted. Due to the reverse-tapered shape of the aneurysm neck, the graft sustained a disposition 6 mm distally leading to an endoleak type I formation. Despite the application of a balloon inflation in the aneurysm neck, the endoleak did not resolve, so a proximal aortic cuff 34 mm in diameter was additionally deployed. Balloon remodeling was performed to the proximal and distal landing zones as well as to all overlapping sites according to the manufacturer's recommendations. Completion angiography revealed adequate graft interposition with exclusion of the aneurysm sac, maintenance of internal iliac arteries' perfusion, and no signs of endoleak. Total operative time was approximately 95 minutes. The patient had no intraoperative complications and remained hemodynamically stable throughout the operation.
Immediately after the procedure, the patient complained for slight global pain in both legs without any moving disability. The same evening as the patient was trying to mobilize, he experienced gait difficulty. Neurologic examination revealed bilateral lower extremity distal paraparesis involving mostly the posterior tibial group of muscles with decreased sensation mainly at 3-4 lower sacral segments on pinprick and sparing light touch. Bladder function was also lost. Urgent magnetic resonance imaging did not reveal evidence of cord compression, hematoma, or infarction. Immediately aggressive diuresis treatment was started. Intravenous solumedrol (5.4 mg/Kg bolus and 30 mg/kg drip) and mannitol (100 mL of 20% solution bolus, followed by 50 mL 4 times daily) were administered. Blood pressure was optimized with intravenous fluids, and mean arterial pressure was kept above 90 to 100 mm Hg. The aggressive diuresis treatment was continued for three days and moderate improvement was noted at neurological examination. The patient was discharged at the 7th postoperative day with no further complications. He followed a long rehabilitation programme and at the one-year followup has regained nearly fully walking ability but retained permanent bladder incontinence. No aneurysm related complications were recorded.
OUTPUT:
| PMC3135247 |
MultiCaRe_Reasoning96408 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 6.0
Sex: Male
Title: Case report: training neck and head control in children with chronic paralysis due to acute flaccid myelitis
Keywords: activity based restorative therapy; acute flaccid myelitis; case series; head and neck control; spinal cord injury;
Abstract:
Background:
Acute flaccid myelitis (AFM) occurs rarely in children and adolescents when damage to spinal motor neurons rapidly causes flaccid paralysis of limb, trunk, and neck muscles and potentially respiratory failure. When neck muscles are weakened or paralyzed, a child loses head control, severely compromising engagement with their environment. Compensation for lack of head control is achieved with external support devices attached to a wheelchair, but there is no indication in the AFM literature of therapeutic efforts to restore head control. In this case series, we explore the possibility of the recovery of head control when children with AFM received activity-based restorative therapies (ABRTs) guided by principles targeting motor control.
Case description:
Three children, two male and one female, aged 6, 9, and 7, with a history of AFM-onset at 5, 7, and 4 years respectively, enrolled in an activity-based restorative therapies outpatient program targeting activation of the neuromuscular system below the lesion. Each of them lacked head control, was either ventilator-dependent or had a tracheostomy, and was a power wheelchair user via hand/foot control.
Methods:
Activity-based restorative therapies were provided 5 days/week: 1.5 h of activity-based locomotor training and 1.5 h of activity-based neuromuscular electrical stimulation.
Results:
An approach to addressing head/neck control developed iteratively across disciplines, from complete compensation with passive external head support to emerging head control during diverse tasks, e.g., sitting, reaching, driving a power chair, sit-to-stand, standing, stepping on a treadmill, and walking. Key principles identified and employed were (a) passive facilitation, (b) external head support, (c) posterior head support, (d) graded manual facilitation, and (e) independent head control.
Discussion:
The recovery of head control in children with paralysis due to AFM may be accelerated when executing a step-wise progression to effectively target and challenge head control in parallel with activity-based restorative therapies. In treating three children with a chronic lack of head control, a therapeutic strategy was iteratively developed guided by scientific principles, e.g., segmental assessment of control, to promote recovery of head control. While this strategy is encouraging, gaps in sensitive and responsive measurement instruments and treatment technologies persist in guiding assistance, challenging, and promoting independent head control.
Image Caption and Description:
Image caption: (A) Timeline from onset of injury at 5 years of age. Patient initiated activity-based restorative therapy (ABRT) at 6 years, 6 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. AFM, acute flaccid myelitis; SATCo, segmental assessment of trunk control. (B) Timeline from onset of injury at 8 years of age. Patient initiated activity-based restorative therapy (ABRT) at 9 years, 6 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. (C) Timeline from onset of injury at 4 years of age. Patient initiated activity-based restorative therapy (ABRT) at 7 years, 5 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. (D) "I can see the ground and around my chair better". This was reported by patient 1 with the transition of external head support from passive capital extension via a headrest (D1) to the implementation of an external head support device promoting midline cervical positioning and the initiation of cervical rotation (D2). (E) Initial vs. final mobility. (E1) Initial mobility presents as seated in power wheelchair in a forward flexed, kyphotic posture, with left lateral cervical flexed positioning. (E2) Final mobility with patient independently controlling posterior walker with bilateral upper extremity platforms. Patient presents with a more upright posture and head toward the midline position. (F) Independent sitting without trunk support vs. manual facilitation of trunk support at the head, trunk, and pelvis. (F1) Without head, trunk, or pelvic support, the patient presents with left lateral cervical flexion, uneven shoulder elevation (left above right), right kyphosis of the rib cage, left lateral trunk flexion, and a left pelvic obliquity. (F2) Manual facilitation was provided at the head, trunk, and pelvis, positioning the patient as close to the midline position as possible. Maximal assistance is required to achieve the positioning in image (F2). (G) Patient demonstrates ambulation with maximal manual facilitation for head support. Without trunk support, he is unable to maintain the trunk and pelvis in midline alignment. Able to ambulate for over 2 min with head support. (H) Able to hold head without manual facilitation at head, trunk, and pelvis in sitting and standing for 2 min each, transitioned from sitting to standing without manual support with inappropriate kinematics of head, trunk, and pelvis.
Image description: AFM diagnosis. At the initial evaluation, the patient was ventilator-dependent and was treated by an outpatient pulmonary rehab team once a week to address sprinting/weaning (Figure 1C).
With manual head support, the patient could sit, perform sit-to-stand, and ambulate, though with an asymmetrical trunk posture (Figure 1G).
Image caption: Initial and final outcomes across all three patients for head control, scoliosis, SATCo, timed sit, timed stand, sit outside base of support, and sit to stand.
Image description: With full support and alignment of the pelvis and trunk in the neutral position, the patient could not control his head, resulting in cervical flexion or extension (Figure 2).
Case Report:
Patient K478, a 6-year-old male enrolled in the Pediatric NeuroRecovery Program 10 months post AFM diagnosis (Figure 1A). At the initial evaluation, he was ventilator-dependent and used a power wheelchair with a left-handed joystick, a passive headrest promoting capital extension (Figure 1D1), and lateral supports for trunk positioning. The patient was non-ambulatory. Outside of the wheelchair and with full manual head support, the patient was able to sit with an anterior pelvic tilt, lumbar lordosis, and upper thoracic extension. With full support and alignment of the pelvis and trunk in the neutral position, the patient could not control his head, resulting in cervical flexion or extension (Figure 2). Without head control in sitting, the resting position of the head was capital extension. The patient experienced a high degree of anxiety toward manual facilitation of head control with the removal of passive support. Prior to enrollment in the Pediatric NeuroRecovery program, the patient received inpatient and outpatient therapy; however, interventions did not specifically address head control. Additionally, head control was managed via passive positioning using a headrest.
OUTPUT:
| PMC10235686 |
MultiCaRe_Reasoning96409 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 9.0
Sex: Female
Title: Case report: training neck and head control in children with chronic paralysis due to acute flaccid myelitis
Keywords: activity based restorative therapy; acute flaccid myelitis; case series; head and neck control; spinal cord injury;
Abstract:
Background:
Acute flaccid myelitis (AFM) occurs rarely in children and adolescents when damage to spinal motor neurons rapidly causes flaccid paralysis of limb, trunk, and neck muscles and potentially respiratory failure. When neck muscles are weakened or paralyzed, a child loses head control, severely compromising engagement with their environment. Compensation for lack of head control is achieved with external support devices attached to a wheelchair, but there is no indication in the AFM literature of therapeutic efforts to restore head control. In this case series, we explore the possibility of the recovery of head control when children with AFM received activity-based restorative therapies (ABRTs) guided by principles targeting motor control.
Case description:
Three children, two male and one female, aged 6, 9, and 7, with a history of AFM-onset at 5, 7, and 4 years respectively, enrolled in an activity-based restorative therapies outpatient program targeting activation of the neuromuscular system below the lesion. Each of them lacked head control, was either ventilator-dependent or had a tracheostomy, and was a power wheelchair user via hand/foot control.
Methods:
Activity-based restorative therapies were provided 5 days/week: 1.5 h of activity-based locomotor training and 1.5 h of activity-based neuromuscular electrical stimulation.
Results:
An approach to addressing head/neck control developed iteratively across disciplines, from complete compensation with passive external head support to emerging head control during diverse tasks, e.g., sitting, reaching, driving a power chair, sit-to-stand, standing, stepping on a treadmill, and walking. Key principles identified and employed were (a) passive facilitation, (b) external head support, (c) posterior head support, (d) graded manual facilitation, and (e) independent head control.
Discussion:
The recovery of head control in children with paralysis due to AFM may be accelerated when executing a step-wise progression to effectively target and challenge head control in parallel with activity-based restorative therapies. In treating three children with a chronic lack of head control, a therapeutic strategy was iteratively developed guided by scientific principles, e.g., segmental assessment of control, to promote recovery of head control. While this strategy is encouraging, gaps in sensitive and responsive measurement instruments and treatment technologies persist in guiding assistance, challenging, and promoting independent head control.
Image Caption and Description:
Image caption: (A) Timeline from onset of injury at 5 years of age. Patient initiated activity-based restorative therapy (ABRT) at 6 years, 6 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. AFM, acute flaccid myelitis; SATCo, segmental assessment of trunk control. (B) Timeline from onset of injury at 8 years of age. Patient initiated activity-based restorative therapy (ABRT) at 9 years, 6 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. (C) Timeline from onset of injury at 4 years of age. Patient initiated activity-based restorative therapy (ABRT) at 7 years, 5 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. (D) "I can see the ground and around my chair better". This was reported by patient 1 with the transition of external head support from passive capital extension via a headrest (D1) to the implementation of an external head support device promoting midline cervical positioning and the initiation of cervical rotation (D2). (E) Initial vs. final mobility. (E1) Initial mobility presents as seated in power wheelchair in a forward flexed, kyphotic posture, with left lateral cervical flexed positioning. (E2) Final mobility with patient independently controlling posterior walker with bilateral upper extremity platforms. Patient presents with a more upright posture and head toward the midline position. (F) Independent sitting without trunk support vs. manual facilitation of trunk support at the head, trunk, and pelvis. (F1) Without head, trunk, or pelvic support, the patient presents with left lateral cervical flexion, uneven shoulder elevation (left above right), right kyphosis of the rib cage, left lateral trunk flexion, and a left pelvic obliquity. (F2) Manual facilitation was provided at the head, trunk, and pelvis, positioning the patient as close to the midline position as possible. Maximal assistance is required to achieve the positioning in image (F2). (G) Patient demonstrates ambulation with maximal manual facilitation for head support. Without trunk support, he is unable to maintain the trunk and pelvis in midline alignment. Able to ambulate for over 2 min with head support. (H) Able to hold head without manual facilitation at head, trunk, and pelvis in sitting and standing for 2 min each, transitioned from sitting to standing without manual support with inappropriate kinematics of head, trunk, and pelvis.
Image description: AFM diagnosis. At the initial evaluation, the patient was ventilator-dependent and was treated by an outpatient pulmonary rehab team once a week to address sprinting/weaning (Figure 1C).
With manual head support, the patient could sit, perform sit-to-stand, and ambulate, though with an asymmetrical trunk posture (Figure 1G).
Case Report:
Patient K491, a 9-year, 6-month-old female enrolled in the Pediatric NeuroRecovery Program 2.5 years post AFM diagnosis. At the initial evaluation, she had a capped tracheotomy and was ventilator-free. The patient arrived in a power wheelchair with a headrest, controlled by a left-handed joystick. The patient typically sat with forward trunk flexion and left lateral cervical flexion, with intermittent use of the headrest (Figure 1E1). She had a severe neuromuscular scoliosis presenting as kyphosis of the right rib cage, cervical and thoracic spine rotation, off-center head positioning (left lateral flexion), left pelvic obliquity, and left lateral trunk lean/collapse of the rib cage. Positioning the patient was challenging due to hypersensitivity to tactile input and severe kyphoscoliosis (Figure 1F1). With manual facilitation at the trunk, she sat with improved alignment, but scoliosis prevented midline positioning in and out of her wheelchair (Figure 1F2). The patient maintained static head positioning independently, with inappropriate alignment (head and trunk postures were not typically aligned) in independent sitting. With manual facilitation positioning the trunk and pelvis as close to the midline as achievable, the patient could not independently maintain head control. She could stand with manual facilitation at the trunk, approximating midline position, and manual head support. The patient was ambulatory with an anterior rolling walker with platform support, though with severely altered alignment of the head and trunk at a therapeutic level. Prior to enrollment in the Pediatric NeuroRecovery program, the patient received inpatient and outpatient therapy; however, interventions did not specifically address head control. Additionally, head control was managed via passive positioning using a headrest. The patient was seen for consultation by a pediatric orthopedic surgeon to monitor the scoliosis relative to any respiratory compromise, functional decline, and quality of life.
OUTPUT:
| PMC10235686 |
MultiCaRe_Reasoning96410 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 7.0
Sex: Male
Title: Case report: training neck and head control in children with chronic paralysis due to acute flaccid myelitis
Keywords: activity based restorative therapy; acute flaccid myelitis; case series; head and neck control; spinal cord injury;
Abstract:
Background:
Acute flaccid myelitis (AFM) occurs rarely in children and adolescents when damage to spinal motor neurons rapidly causes flaccid paralysis of limb, trunk, and neck muscles and potentially respiratory failure. When neck muscles are weakened or paralyzed, a child loses head control, severely compromising engagement with their environment. Compensation for lack of head control is achieved with external support devices attached to a wheelchair, but there is no indication in the AFM literature of therapeutic efforts to restore head control. In this case series, we explore the possibility of the recovery of head control when children with AFM received activity-based restorative therapies (ABRTs) guided by principles targeting motor control.
Case description:
Three children, two male and one female, aged 6, 9, and 7, with a history of AFM-onset at 5, 7, and 4 years respectively, enrolled in an activity-based restorative therapies outpatient program targeting activation of the neuromuscular system below the lesion. Each of them lacked head control, was either ventilator-dependent or had a tracheostomy, and was a power wheelchair user via hand/foot control.
Methods:
Activity-based restorative therapies were provided 5 days/week: 1.5 h of activity-based locomotor training and 1.5 h of activity-based neuromuscular electrical stimulation.
Results:
An approach to addressing head/neck control developed iteratively across disciplines, from complete compensation with passive external head support to emerging head control during diverse tasks, e.g., sitting, reaching, driving a power chair, sit-to-stand, standing, stepping on a treadmill, and walking. Key principles identified and employed were (a) passive facilitation, (b) external head support, (c) posterior head support, (d) graded manual facilitation, and (e) independent head control.
Discussion:
The recovery of head control in children with paralysis due to AFM may be accelerated when executing a step-wise progression to effectively target and challenge head control in parallel with activity-based restorative therapies. In treating three children with a chronic lack of head control, a therapeutic strategy was iteratively developed guided by scientific principles, e.g., segmental assessment of control, to promote recovery of head control. While this strategy is encouraging, gaps in sensitive and responsive measurement instruments and treatment technologies persist in guiding assistance, challenging, and promoting independent head control.
Image Caption and Description:
Image caption: (A) Timeline from onset of injury at 5 years of age. Patient initiated activity-based restorative therapy (ABRT) at 6 years, 6 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. AFM, acute flaccid myelitis; SATCo, segmental assessment of trunk control. (B) Timeline from onset of injury at 8 years of age. Patient initiated activity-based restorative therapy (ABRT) at 9 years, 6 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. (C) Timeline from onset of injury at 4 years of age. Patient initiated activity-based restorative therapy (ABRT) at 7 years, 5 months old. Arrows indicate the therapies patient was receiving and the number of times per week they participated. (D) "I can see the ground and around my chair better". This was reported by patient 1 with the transition of external head support from passive capital extension via a headrest (D1) to the implementation of an external head support device promoting midline cervical positioning and the initiation of cervical rotation (D2). (E) Initial vs. final mobility. (E1) Initial mobility presents as seated in power wheelchair in a forward flexed, kyphotic posture, with left lateral cervical flexed positioning. (E2) Final mobility with patient independently controlling posterior walker with bilateral upper extremity platforms. Patient presents with a more upright posture and head toward the midline position. (F) Independent sitting without trunk support vs. manual facilitation of trunk support at the head, trunk, and pelvis. (F1) Without head, trunk, or pelvic support, the patient presents with left lateral cervical flexion, uneven shoulder elevation (left above right), right kyphosis of the rib cage, left lateral trunk flexion, and a left pelvic obliquity. (F2) Manual facilitation was provided at the head, trunk, and pelvis, positioning the patient as close to the midline position as possible. Maximal assistance is required to achieve the positioning in image (F2). (G) Patient demonstrates ambulation with maximal manual facilitation for head support. Without trunk support, he is unable to maintain the trunk and pelvis in midline alignment. Able to ambulate for over 2 min with head support. (H) Able to hold head without manual facilitation at head, trunk, and pelvis in sitting and standing for 2 min each, transitioned from sitting to standing without manual support with inappropriate kinematics of head, trunk, and pelvis.
Image description: AFM diagnosis. At the initial evaluation, the patient was ventilator-dependent and was treated by an outpatient pulmonary rehab team once a week to address sprinting/weaning (Figure 1C).
With manual head support, the patient could sit, perform sit-to-stand, and ambulate, though with an asymmetrical trunk posture (Figure 1G).
Image caption: Outline of the steps developed over time to address and progress head control as patient control increased across time..
Image description: During overground and activity-based occupational therapy, an external head device called a HeadPod assisted in providing head support (Figures 3, 4A).
Graded manual facilitation was introduced via a segmental approach at the C1-C7 vertebrae (Figures 3, 4A).
Image caption: (A) Progression of head control. Passive manual facilitation provided at the head due to no head control outside of chair/headrest. External head support device in place providing maximal assistance at the head. External head support device allows for patient initiation of cervical flexion, extension, and rotation. Posterior head support was provided to the head and trunk to address upright stabilization of head control in a vertical position with maximal assistance at the trunk and pelvis for midline positioning. As midline stabilization was achieved with posterior support, the patient transitioned to addressing cervical lateral flexion, flexion, and rotation with posterior support. Graded manual facilitation from C1 to C7 with improved head control initiation, graded from distal to proximal until support was able to be removed from head/neck. With increased activation of cervical musculature, increased head control was observed with support; the posterior support was removed and training transitioned to head control without manual facilitation. Assistance was graded over time pending each patient's progress and strengths. Grading included moving from distal to more proximal support until head and/or trunk support could be removed. (B) Progression of trunk control. Initial SATCo demonstrated no head control across all three patients. Patients 1 and 3 required manual facilitation at the head for initial SATCo. Final SATCo demonstrated increased head control across all three participants, with a change in the scores of patient 2, demonstrating static head control. Patients 1 and 3 presented with emerging control toward static head control. Patient 1 demonstrated head control without manual facilitation at the final SATCo.
Image description: During overground and activity-based occupational therapy, an external head device called a HeadPod assisted in providing head support (Figures 3, 4A).
As cervical musculature activation progressed, head control facilitation transitioned from maximal manual facilitation to the implementation of a posterior surface in sitting/standing (Figure 4A).
As head control progressed, the posterior support was removed (Figure 4A) and the head control goal shifted to achieve midline positioning without occipital support.
Graded manual facilitation was introduced via a segmental approach at the C1-C7 vertebrae (Figures 3, 4A).
Case Report:
Patient K1014, a 7-year, 5-month-old male enrolled in the Pediatric NeuroRecovery Program 3.5 years post AFM diagnosis. At the initial evaluation, the patient was ventilator-dependent and was treated by an outpatient pulmonary rehab team once a week to address sprinting/weaning (Figure 1C). The patient arrived in a power wheelchair driven with right foot control, with the head in a passive support promoting capital extension and bilateral lateral trunk supports. The patient presented with a flexible scoliosis and a tendency toward a right lateral lean; however, midline positioning was achieved with manual facilitation. The patient received compensatory bracing typically associated with scoliosis, thoracic-lumbar-sacral orthosis; however, he did not receive surgical intervention. With the head support, the patient could move through partial lateral cervical flexion when sitting or standing. With manual head support, the patient could sit, perform sit-to-stand, and ambulate, though with an asymmetrical trunk posture (Figure 1G). Prior to enrollment in the Pediatric NeuroRecovery program, the patient received inpatient and outpatient therapy; however, interventions did not specifically address head control. Additionally, head control was managed via passive positioning using a headrest.
The activity-based restorative therapies program's objective is to activate the neuromuscular system below the lesion to promote task-specific kinematics during repetitive training targeting recovery-based movement without compensatory strategies. Physical therapy and occupational therapy followed activity-based restorative therapies principles: (a) maximize weight-bearing on the legs; (b) optimize sensory cues specific to the tasks, for example, standing and stepping; (c) optimize trunk, pelvis, and limb kinematics associated with specific motor tasks; and (d) maximize recovery strategies and minimize compensation strategies.
The training protocol was developed using current trunk and head control literature available on SCI, Cerebral Palsy, and an iterative approach to addressing head control deficits (Figure 3).
A team of four Physical Therapists (LLM, MGR, MD, and SS) and two Occupational Therapists (DS and KN) treated these three patients. Weekly staff meetings provided time for formal discussions of treatment strategies, while informal team interaction during patient therapy sessions allowed for collaboration and trials of new strategies. While ABRT principles provided a foundation for activating the neuromuscular system serving neck and head control, steps to grade task difficulty, i.e., easier or more difficult, were made inherently with each transition to a more challenging environment or control requirement for task performance. Thus, challenging the system was a necessity for the progression of skill. These objectives were revisited throughout each child's stay as we learned more about ways to facilitate continued use of control gains in and outside of therapy.
Patients were initially provided trunk and pelvic support to position the trunk in midline alignment and the pelvis neutrally in a 90/90/90 seated position. The level of trunk support was determined using SATCo scores to allow isolated activation and targeting of the cervical musculature with the patient outside of their wheelchair. As patients progressed, trunk support was graded by height or amount of support to increase the challenge for trunk and head control. Key prompts/cues used throughout head control interventions included visual feedback via a mirror or video for patients to visualize their total body positioning, modeling, manual facilitation, and verbal cues.
Throughout the activity-based locomotor training, various devices were implemented, with an emphasis on providing head support for positioning in the dynamic treadmill environment. During overground and activity-based occupational therapy, an external head device called a HeadPod assisted in providing head support (Figures 3, 4A). The HeadPod provided dynamic support without limiting cervical rotation. This device allowed for patient activation of cervical stabilizers while decreasing passive support.
The following highlights key principles identified and implemented in daily treatment sessions to address head control progression.
Initial head control training used manual facilitation and/or external head support with the head in the midline position. The intention was to decrease sensitization to passive head control positioning in the midline position, seated outside of the wheelchair, to improve proprioception (patient recognition and awareness) of midline head positioning, and to provide opportunities for the initiation of head movement with a stable base of support and maximal assistance at the head/neck. The role of the therapist was to provide a safe and encouraging environment to address the activation of the cervical musculature with appropriate cervical, trunk, pelvis, and body kinematics. This allowed the patient to initiate the activation of cervical musculature in a position of proper alignment with the body. The therapist further assisted the patient by understanding where their body was in space and understanding the midline head position in an upright seated position. The therapist further facilitated proprioception and cervical activation via the active assisted range of motion of cervical rotation, lateral flexion, extension, and flexion, with the patient learning to initiate the movement. This step emphasizes cervical musculature activation with a minimum of trace movement achieved prior to initiating the next step.
As cervical musculature activation progressed, head control facilitation transitioned from maximal manual facilitation to the implementation of a posterior surface in sitting/standing (Figure 4A). Stabilizing the head in space, on the posterior surface, is one strategy used to provide a stable, vertical position reference. This control is essential for anticipating and adapting balance control.
This posterior surface extended from the sacral spine to the occiput. The patient worked to maintain their head against the surface in the midline position, pull the head away from the surface, and perform rotation and lateral flexion/extension. Initially, the therapist would provide cues to grade head movement through a specific range of motion using the posterior support. For example, therapists may provide five-degree incremental boundaries for loss of control. If the patient lost control of their head in left lateral flexion, a boundary or cues were provided by the therapist to grade the loss of control and then allow the patient the opportunity to initiate right lateral flexion to return their head to the midline position. Grading the activity was essential to increase motivation and participation on the patient's behalf. When therapists facilitated the incremental range of motion (5 -10 ) from the midline position, patients saw improved voluntary transitions back to the midline position. Without therapist assistance, patients would typically lose full control of this transition, requiring maximal assistance for safety and to return to the midline position. We observed that each child achieved control of the head in the midline position against a posterior support for thirty seconds or more in advance of "graded manual facilitation".
As head control progressed, the posterior support was removed (Figure 4A) and the head control goal shifted to achieve midline positioning without occipital support. Graded manual facilitation was introduced via a segmental approach at the C1-C7 vertebrae (Figures 3, 4A). This approach is comparable to that used to facilitate gains in trunk control in children lacking trunk control (the Segmental Assessment of Trunk Control). Similarly, we used biomechanical levels of the cervical spine to provide manual support upon a stable base, neutral pelvis, and supported trunk. Manual support moved in a cephalad to caudal direction at cervical spine segments as the patient's static control of the head/neck improved. The role of the therapist was to alter the placement of support along the cervical spine until full static head control was achieved without support. This indicated that the patient was prepared for the next step toward "independent head control".
Independent head control is defined by the removal of hands-on support or manual facilitation from the head/neck, with or without manual facilitation at the trunk. Each patient progressed differently throughout the progression of head control interventions. However, in this step, some patients performed independent head control without trunk support in sitting and standing, while others required maximal trunk support in sitting to maintain independent head control.
The therapist's role was to grade the intervention and determine when patients were appropriate to trial independent head control in sitting vs. standing and/or with/without trunk support. This activity often engaged a collaborative partnership, with the patient voicing their capacity and, thus, their willingness to trial different tasks and positions during head control. Interventions in this stage included stationary sitting, sitting outside the base of support, transitioning from trunk flexion or extension to midline, sit to stand, stationary standing, and ambulation.
OUTPUT:
| PMC10235686 |
MultiCaRe_Reasoning96411 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 65.0
Sex: Female
Title: Bilateral breast carcinoma- a rare case report
Keywords: breast; carcinoma; chemotherapy; mastectomy; synchronous; ultrasonography;
Abstract:
We are presenting a rare case of bilateral breast cancer. A 65-year-old female reported to us with complaint of lump in the left breast. There was positive family history. The patient was diagnosed with carcinoma breast of left side on edge biopsy and of right side by ultrasonography, which was confirmed on fine needle aspiration cytology. At the time of admission, ultrasonography of the abdomen and right breast were normal. After 1 month, the patient was readmitted with redness over the inner quadrant of the right breast skin.
Image Caption and Description:
Image caption: Gross picture showing operated site on left breast and redness over the right breast region
Image description: On right side of breast, skin was reddish in colour in lower and inner quadrant but no lump was felt (Figure 1).
Case Report:
Case report-A 65 year-old woman came to our Breast unit due to a palpable lesion in her left breast. From the personal history, the woman had risk factors of positive family history for breast cancer. Her mother was diagnosed with breast cancer of right side. There were no other complaints like weight loss, fever or loss of appetite.
Clinical examination of the left breast revealed a hard lump in the upper quadrant of size 14 x 10 cm that was fixed to the underlying structures. The overlying skin of the breast along with nipple and areola were involved. Multiple lymph nodes were felt in the axilla, out of which one was large in size-of about 2x3cm, which was mobile.
On right side of breast, skin was reddish in colour in lower and inner quadrant but no lump was felt (Figure 1). Nipple was inverted. No axillary lymph nodes were felt. Routine blood tests were within normal limits including chest X-ray.
In ultrasound of the left breast, the consistency of the lesion was solid and multilobular. Additionally, ultrasonography of the right breast demonstrated a non-palpable lesion, consisting of clustered micro calcifications of a diameter equal to 0.7 cm in the upper outer quadrant. Abdominal ultrasonography revealed no metastasis. Fine needle aspiration cytology confirmed the malignancy of both breasts. On the right side, it came as invasive lobular carcinoma and on the left side, it came as ductal carcinoma. Modified radical mastectomy with axillary clearance and skin grafting was performed on the left breast. Pathological specimen showed a large well-demarcated tumour mass measuring 14 x 10 x 9 cm, firm to hard in consistency. Histopathological examination confirmed the diagnose of ductal carcinoma with lymph node infiltration. Specimen revealed 9 lymph nodes. Post-operatively, the patient was on adjuvant chemotherapy and responded very well to the treatment.
OUTPUT:
| PMC3056428 |
MultiCaRe_Reasoning96412 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 46.0
Sex: Male
Title: Tuberculosis of the adrenal gland: a case report and review of the literature of infections of the adrenal gland
Keywords: None
Abstract:
Infections of the adrenal glands remain an important cause of adrenal insufficiency, especially in the developing world. Indeed, when Thomas Addison first described the condition that now bears his name over 150 years ago, the vast majority of cases were attributable to tuberculosis. Here we describe a classic, but relatively uncommon, presentation in the United States of adrenal insufficiency followed by a review of the current literature pertaining to adrenal infections.
Image Caption and Description:
Image caption: CT scan of the abdomen and pelvis with oral and intravenous contrast showing bilateral adrenal enlargement (black arrows).
Image description: A computed tomography scan of the abdomen with intravenous contrast revealed bilaterally enlarged adrenal glands (4 cm x 3.3 cm on the right, 2.3 cm x 2.1 cm on the left) (Figure 1).
Case Report:
A 46-year-old man presented to his physician with a 3-month history of generalized weakness and 15-pound unintentional weight loss. He also reported mild dyspnea on exertion and decreased appetite. His past medical history was significant for hypertriglyceridemia, primary hypothyroidism, and vitamin D deficiency. He had emigrated from the Philippines 6 years prior and had been working as a nurse at a skilled nursing facility. He had not left the country since his initial arrival. He denied sick contacts, specifically exposure to tuberculosis, smoking, alcohol consumption, or the use of illicit substances. A tuberculin skin test performed in 2007 resulted in induration (diameter unknown) and it was attributed to prior BCG vaccine. There was no evidence of pulmonary tuberculosis on a chest radiograph. Physical examination revealed abdominal distension and free fluid but was otherwise unremarkable. A diagnostic paracentesis revealed an exudative effusion with a positive Ziehl Neelsen stain for acid fast bacilli. The patient was started on treatment (Isoniazid, rifampicin, pyrazinamide, and ethambutol) for presumed extrapulmonary tuberculosis which was later confirmed by culture.
One month after starting antitubercular therapy he presented to the hospital with worsening fatigue, salt craving, vomiting, loss of libido, and erectile dysfunction. On examination, he had low blood pressure and appeared cachectic. In addition he had bitemporal muscle wasting and hyperpigmentation of skin, oral mucosa, and nails. Laboratory evaluation was significant for hyponatremia, hyperkalemia, and mild hypercalcemia. A random cortisol was 2.5 mcg/dL with an ACTH of 531.2 pcg/mL. The basal and cosyntropin stimulated serum cortisol were, respectively 1.8 mcg/dL and 2.0 mcg/dL, which was consistent with the diagnosis of primary adrenal insufficiency most likely due to tuberculosis. A computed tomography scan of the abdomen with intravenous contrast revealed bilaterally enlarged adrenal glands (4 cm x 3.3 cm on the right, 2.3 cm x 2.1 cm on the left) (Figure 1). On review of his prior CT scan of the abdomen, the patient had bilaterally enlarged adrenal glands at the time of his initial presentation as well.
With the background of tuberculosis and acute adrenal insufficiency diagnosed by laboratory test, bilateral enlargement of adrenal glands was considered most consistent with tuberculosis in our patient. Deterioration of his clinical status following antitubercular treatment could be attributed to accelerated cortisol metabolism by induction of CYP 3A4 by rifampicin. He was initially treated with intravenous hydrocortisone and was subsequently discharged on hydrocortisone and fludrocortisone. His symptoms have improved significantly. However, he is requiring slightly higher dose of hydrocortisone, which could be due to CYP 3A4 induction by rifampicin. He is likely to require lifelong treatment for adrenal insufficiency. A study that looked at tuberculosis patients with bilaterally enlarged adrenal glands found that treatment with antituberculosis drugs does not improve or help recover adrenal functionality. Adrenal biopsy was not performed because the presentation was strongly suggestive of adrenal tuberculosis with active extra-adrenal tuberculosis.
Comment. It is to be noted that BCG vaccine received at birth has no impact on PPD test result 10 years later. The presumption made by the other hospital that this patient's positive TST is secondary to a vaccination at birth was incorrect. Positive PPD in this patient should have prompted further investigations.
It is interesting to note that Thomas Addison was in fact seeking an anatomic basis for pernicious anemia rather than the biochemical effects of adrenal insufficiency when he published his seminal paper on the subject. The eleven patients he described in his report all had tuberculosis of the adrenal glands. This consumption has since receded to the background of ailments that afflict the Western world and today is generally considered a disease of immigrants from endemic areas, the immunocompromised or the destitute. In the developing world, however, tuberculosis continues to account for about 20-30% of cases of Addison's disease.
The clinical presentation of primary adrenal insufficiency is protean, and an underlying infectious etiology can further obscure the manifestations. The most frequent manifestations are weakness, fatigue, anorexia, weight loss, nausea, vomiting, hypotension, and skin hyperpigmentation (present in 60-100% of patients). Understandably any of the above symptoms or signs could be easily missed or attributed to the primary infectious process itself.
In the developed world, about 10% of cases of Addison's disease have an infectious etiology; however there are few data available regarding the frequency of organisms that cause clinical adrenal insufficiency. HIV/AIDS and opportunistic infections like cytomegalovirus are the most commonly cited causes following tuberculosis. Various fungi like Cryptococcus, Histoplasma, Coccidioides, Paracoccidioides are also described to involve the adrenal glands in several case reports (Table 1).
Mycobacterium tuberculosis complex spreads to the adrenal glands hematogenously. Clinical manifestations may take years to become apparent, and asymptomatic infection is not uncommon. Adrenal involvement was found in 6% of patients with active tuberculosis in an autopsy series. More than 90% of the gland must be destroyed before insufficiency appears. The widespread use of computed tomography has improved our understanding of the patterns of involvement of the adrenal gland in tuberculosis. The majority of patients with active or recently acquired disease (<2 years) have bilateral adrenal enlargement, while calcification and atrophy are the norm with more remote infection or inactive disease.
That the adrenals can be enlarged in patients with pulmonary tuberculosis without active involvement of the glands has been demonstrated in various studies. Stress and inflammation could be potential reasons. The activity of the hypothalamic pituitary axis (HPA) has been the subject of numerous studies. The lack of a uniform definition of a "normal cortisol response" to ACTH stimulation has perhaps contributed to some of the heterogeneity in the results. Kelestimur et al. studied the HPA axis in 27 patients with active pulmonary tuberculosis. They also compared responses to 1 mcg and 250 mcg ACTH stimulation. Cortisol responses were consistently higher in the cases when compared to controls. A more recent study by Laway et al. found significantly lower basal and stimulated cortisol levels in active pulmonary tuberculosis when compared to controls, as well as enlarged adrenal glands. None of the patients had clinical adrenal insufficiency. Both of these findings improved after successful antituberculous treatment. However, the absence of serum albumin levels and the lack of adrenal biopsies in the cases limit the interpretation of the results. Other studies have also demonstrated a reduction in adrenal gland size after successful treatment of pulmonary tuberculosis.
When tuberculosis results in overt adrenal insufficiency, antituberculous chemotherapy does not appear to restore function. One must also be cognizant of the effect of rifampin, a potent hepatic enzyme inducer on the metabolism of glucocorticoids. Failure to increase the dose of steroid replacement therapy may result in the development of adrenal crisis. Adrenal biopsy is not necessary for primary adrenal insufficiency with bilateral adrenal enlargement in a patient with proven extra-adrenal tuberculosis. However, about 12% of patients with adrenal tuberculosis have no evidence of active extra-adrenal tuberculosis. Adrenal biopsy is generally necessary in these patients to prove adrenal involvement by tuberculosis.
HIV infection affects the adrenal gland in multiple ways. Apart from direct infection, opportunistic infections and antiretroviral medications also have a significant effect on the adrenal glands.
Adrenal insufficiency is prevalent in 17% of patients admitted with AIDS. Due to its high prevalence, recommendations have been made to screen for adrenal insufficiency in HIV patients with symptoms. Most common causes of adrenal insufficiency are infections like CMV, Mycobacterium tuberculosis and MAI, Cryptococcus neoformans, Histoplasma capsulatum, Pneumocystis jirovecii, and Toxoplasma gondii, neoplastic diseases (Kaposi's sarcoma and lymphoma), and bilateral adrenal hemorrhage. Few drugs used for the treatment of HIV infection (protease inhibitors) and drugs used to treat opportunistic infections like rifampicin, ketoconazole, and cotrimoxazole may exacerbate manifestations of primary adrenal insufficiency. Studies have shown decreased level of cortisol, adrenal androgens, and mineralocorticoids in patients infected with HIV.
HIV infection can also lead to secondary adrenal insufficiency in advanced stages of the disease by decreasing pituitary and adrenal responses to CRH. Opportunistic infections like CMV, Mycobacterium tuberculosis, Toxoplasma gondii, Cryptococcus neoformans, and Pneumocystis jirovecii can also infiltrate the pituitary leading to multiple endocrinopathies.
Treatment of adrenal insufficiency in HIV infection includes hydrocortisone and fludrocortisone (if there is evidence of mineralocorticoid insufficiency).
There are cases of Cushing's like phenotype in patients treated with antiretroviral drugs (protease inhibitors and NNRTIs) often referred to as "pseudo-Cushing's". A normal cortisol response to the dexamethasone suppression test differentiates pseudo-Cushing's from Cushing's syndrome. Studies have also shown elevated levels of basal plasma cortisol in untreated HIV patients when compared to healthy individuals. The postulated mechanisms include stress due to HIV infection, increased cytokines resulting in stimulation of HPA axis, and reduction in cortisol catabolism.
Adrenal tumors found almost exclusively in HIV patients include Kaposi's sarcoma which is secondary to coinfection with the oncogenic human herpes virus type 8 (HHV8) and non-Hodgkin's lymphoma (high-grade malignant B phenotype) which could be secondary to Epstein-Barr virus (EBV).
Human cytomegalovirus (HCMV) has been frequently identified as a cause of adrenal insufficiency, especially in patients with HIV/AIDS. The virus has been shown by Trevisan et al. to infect normal human adrenocortical cells and induce cytopathic changes. It also acts as an inducer of steroidogenesis which may explain the discordance between the high rates of CMV adrenalitis in immune suppressed patients in autopsy studies and the relatively rare diagnosis of adrenal insufficiency ante mortem. The virus causes the greatest damage at the cortex-medulla junction. While adrenalitis may be the sole manifestation, the disease is usually disseminated. There have been case reports of exacerbation of CMV infection in patients of adrenal insufficiency after starting glucocorticoids most likely due to the immunosuppressive effect.
Adrenal involvement is typically seen with disseminated chronic histoplasmosis. In one report, primary adrenal insufficiency occurred in 41.3% of adrenal histoplasmosis cases. Histoplasmosis often coexists with HIV-AIDS and is more commonly seen in the immunocompromised, posttransplant and elderly populations. Histoplasmosis presents with similar constellation of clinical features as tuberculosis and is often missed. Furthermore, it also shares pathological characteristics of necrotizing granulomas and caseous necrosis with tuberculosis. Adrenal glands have bilaterally enlarged radiographic appearance and CT guided biopsy often confirms the diagnosis of adrenal histoplasmosis. In addition to tuberculosis, it can also be often mistaken for a lymphoma, underlining the importance of biopsy in these cases. Management includes treatment with amphotericin B followed by itraconazole (for disseminated disease) and replacement of glucocorticoid and mineralocorticoid if there is evidence of adrenal insufficiency.
Paracoccidioides, a thermal dimorphic fungus, causes infection through the inhalation of infectious conidia. It is endemic in several South American countries. Two species, P. braziliensis and P. lutzi, are pathogenic in humans. While the acute form usually appears as progressive lymphadenopathy, the chronic form affects the skin, lungs, mucous membranes, and the adrenal glands. Adrenal insufficiency occurs in a large number of patients (2.9%-48.2%) and has even been reported as the initial presenting feature. Autopsy series have demonstrated adrenal involvement in 85-90% of cases. Clinical manifestations range from the asymptomatic to frank Addisonian crisis. This correlates with the extent of granulomatous involvement of the adrenal glands. Similar to tuberculosis, adrenal insufficiency typically persists even after treatment of the infection.
Many of the herpes viruses infect the adrenal gland including herpes simplex virus types 1 and 2, Epstein-Barr virus, and HCMV. This occurs usually in the setting of disseminated disease and may appear as adrenalitis. Disseminated HSV type 1 and 2 infections in neonates can be fulminant. Murine models suggest the possibility of the adrenals being the initial seat of multiplication of these viruses.
EBV, HCMV, and Polyoma BK virus have been identified in resected adrenocortical tumors; the former has also been associated with lymphoma of the adrenal gland.
Other commonly occurring viruses that can infect the adrenal glands include echoviruses which can lead to adrenal hemorrhage and necrosis in neonates.
The hemorrhagic fever viruses, although rare, can cause devastating damage to the adrenal glands. The Ebola virus, a filovirus, has been shown to cause liquefaction of the adrenals. Other filoviruses and arenaviruses can also damage the adrenals by direct infection.
Adrenal cryptococcosis occurs in disseminated cryptococcal infection, usually in the immunocompromised; however, there are case reports of adrenal cryptococcosis in healthy individuals as well. Pneumonia and meningitis are the most common presentations. Like any other fungal infection, the adrenal glands are enlarged on CT scan and the diagnosis is confirmed by a CT guided biopsy. Cryptococcal antigen titers are invariably high and can be used as a biomarker for disease resolution on follow-up. A 6-month course of fluconazole appears to be effective. In contrast to tuberculosis and histoplasmosis, adrenal insufficiency is often improved with resolution of the disease. Adrenal cryptococcal infection resistant to antifungal therapy may respond to adrenalectomy.
Pneumocystis jirovecii is an infrequent cause of adrenal insufficiency even in patients with defective cell mediated immunity such as patients with HIV/AIDS. However, it has been known to cause fatal adrenal crisis in the apparently immunocompetent host as well.
Blastomyces dermatitidis is a thermal dimorphic fungus that is the North American counterpart of Paracoccidioides in terms of its pathogenesis and propensity for establishing chronic systemic infection. Although pulmonary infection is the most common presentation, it frequently affects the skin, bones, adrenal glands, and the genitourinary system. Almost any organ system may be involved. It appears that subclinical infection of the adrenal glands is more common than overt insufficiency. About 10% of cases in autopsy series revealed adrenal gland infection. Amphotericin B and itraconazole are the drugs of choice in disseminated disease.
Atypical mycobacteria have been isolated from adrenal glands in patients with HIV/AIDS, however, given the multiple etiologies for adrenal insufficiency and frequent coinfection with other organisms that are known to cause destruction of the adrenal glands; however, it is difficult to establish a causal relationship.
The Waterhouse-Friedrichsen syndrome deserves special mention. It is a form of acute adrenal insufficiency that occurs in the setting of bacterial sepsis resulting in adrenal hemorrhage. A number of bacteria are associated with this entity including N. meningitidis, H. influenza, pneumococcus, P. multocida, K. oxytoca, S. aureus, Capnocytophaga canimorsus, Ewingella, and group A streptococcal infections. The organisms are rarely isolated from the adrenal glands at autopsy.
Of all the organisms mentioned in this review, parasites are perhaps the least commonly reported causes of adrenal infection in the United States. Microsporidia have been reported to cause necrotic lesions in the adrenal glands, particularly in patients with AIDS. Echinococcosis (hydatid disease) is responsible for about 7% of all adrenal cysts. Treatment is surgical excision followed by several months of chemotherapy with oral albendazole to prevent recurrence. Visceral leishmaniasis is another cause of cystic adrenal disease. Trypanosoma cruzi, the causative agent of Chagas' disease, has been shown to infect the adrenal gland. Studies have postulated that the adrenals may serve as a reservoir for T. cruzi and parasitemia in the central adrenal vein has been correlated with the development of chronic chagasic cardiomyopathy. African trypanosomiasis has been associated with polyendocrinopathies including hypogonadism, hypothyroidism, and adrenal insufficiency. This can result from a primary glandular or secondary (central) involvement. In one case series of 137 Ugandan patients, treatment of the infection resulted in recovery of adrenal and thyroid function, but hypogonadism tended to persist for years.
OUTPUT:
| PMC4138934 |
MultiCaRe_Reasoning96413 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 26.0
Sex: Male
Title: Primary hepatic neuroendocrine tumor associated with hypertension: A case report
Keywords: case report; hypertension; liver; neuroendocrine tumors; primary;
Abstract:
Background:
Primary neuroendocrine tumors are exceedingly rare and often misdiagnosed. The combined methods of ultrasonography, computed tomography ,and magnetic resonance imaging are typically applied. The diagnosis of the disease mainly depends on the histopathological examination. Surgical resection is the most effective treatment.
Case presentation:
In the report, we describe the case of a patient with a primary hepatic neuroendocrine tumor (PHNET) associated with hypertension. The patient suffered from uncontrolled hypertension before the operation, and the blood pressure was not well controlled by oral antihypertensive drugs such as nifedipine, valsartan, and hydrochlorothiazide, but the patient's blood pressure completely returned to normal after the operation without drug control.
Conclusions:
We encountered a rare case of a PHNET associated with hypertension via careful screening noticed by the patient at work; furthermore, we hope to collect more cases and find the relationship between neuroendocrine tumors and hypertension.
Image Caption and Description:
Image caption: CT and MRI (a round solitary hepatic mass in the left lobe of liver was found, measuring 7.5 cm x 6.1 cm x 6.2 cm, with clear and smooth border and homogeneous density in enhanced scan). CT, computed tomography; MRI, magnetic resonance imaging.
Image description: Enhanced magnetic resonance imaging (MRI) showed an oval mass with a high signal intensity that measured 7.7 cm x 5.1 cm x 6.6 cm (Figure 1).
Case Report:
A 26-year-old male was admitted to Lanzhou University Second Hospital with a 2-year history of hypertension. His blood pressure (BP) went up to 280/170 mmHg, and he needed to take a quadruple dose of antihypertensive drugs to control hypertension. There was no history of hepatitis, Cushing syndrome, diabetes, heart diseases, carcinoids, or other remarkable diseases. In terms of the physical examination, the patient was anicteric with a soft abdomen. The laboratory test results were all normal. The tumor markers alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA), CA19-9, and CA125 were all within normal ranges. The thyroid hormone level is normal. Vanillylmandelic acid (VMA), urine17-ketosteroide (17-ks), and 17-hydroxy-cortico-steroid (17-OHCS) were within normal ranges. The serum cortisol level was normal. With the use of a liver-specific contrast agent, an abdominal contrast-enhanced computed tomography (CT) was performed, and a round, solitary hepatic mass in the left lobe of the liver was observed that measured 7.5 cm x 6.1 cm x 6.2 cm and had a clear and smooth border as well as homogeneous density as seen on the enhanced scan. A proper hepatic artery branch had enveloped the lesion in the arterial phase. There was no evidence of other diseases or lymphatic metastasis. Enhanced magnetic resonance imaging (MRI) showed an oval mass with a high signal intensity that measured 7.7 cm x 5.1 cm x 6.6 cm (Figure 1). An atypical hepatic adenoma was considered. Hypointense and homogenous lesions were shown on preenhanced T1- and T2-weighted images. The Apparent Diffusion Coefficient (ADC) values observed with diffusion-weighted imaging (DWI) were restricted. The lesions appeared to have capsule enhancement in the portal phase and delayed phase, and obvious enhancement washout was observed on the delayed images. Abdominal ultrasound imaging demonstrated a mass in the left lateral segment of the liver, which was defined as hepatic hemangioma. No other occupying lesions were found on systemic CT scan. A diagnosis of hepatic carcinoma (tumor) was made, and further immunohistochemical testing was needed to confirm the type of tumor.
OUTPUT:
| PMC9981943 |
MultiCaRe_Reasoning96414 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 38.0
Sex: Female
Title: SARS during pregnancy, United States
Keywords: None
Abstract:
None
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
The patient, a healthy, 38-year-old woman in the 7th week of pregnancy, traveled with her husband to Hong Kong. From March 1 to March 6, 2003, they stayed at the Hong Kong hotel where it is believed a physician from China spread SARS-CoV to several guests. These guests were the index case-patients for subsequent outbreaks in Hong Kong, Vietnam, Singapore, and Toronto, Canada. The woman and her husband returned to the United States on March 6; the husband had onset of SARS illness on March 13. On March 19, the patient had onset of an illness with fever (temperature 37.8-40 C), muscle aches, chills, headache, runny nose, productive cough, wheezing, and shortness of breath. A chest radiograph showed a diffuse infiltrate in the left lung. The patient was hospitalized for 9 days and given broad-spectrum antimicrobial drugs. She recovered from her illness, and enzyme immunoassay and immunofluorescent assays conducted on serum samples on days 28 and 64 after illness onset were positive for antibodies to SARS-CoV.
The patient had an uneventful pregnancy until the last trimester, when her blood glucose levels were elevated. Early spontaneous rupture of membranes initiated preterm labor, and a cesarean section was performed at 36 weeks' gestation because of fetal distress. A 5-pound, 7-ounce, healthy boy was delivered without complications. Apgar scores were 7 at 1 minute and 8 at 5 minutes. The newborn had no illness, abnormalities, or congenital malformations. Serum samples from the patient at delivery were positive for antibodies to SARS-CoV, but cord blood and placenta samples were negative. Breast milk samples on postpartum days 12 and 30 were also negative for SARS-CoV antibodies. Blood, stool, and nasopharyngeal swab samples from the patient and cord-blood samples showed no viral RNA by reverse transcription-polymerase chain reaction. Stool samples from the newborn, collected on days 12 and 30 after delivery, were also negative for viral RNA.
Although other countries have reported cases of severe illness and poor outcome associated with SARS-CoV infection during pregnancy (-), neither of the two pregnant SARS case-patients in the United States had serious adverse outcomes. The presence of antibodies to SARS-CoV in breast milk might be influenced by the time of infection in relation to gestation. Robertson et al. reported that antibodies to SARS-CoV were detected in the breast milk of a patient who was infected at 19 weeks' gestation; however, the patient in this case was infected at 7 weeks' gestation, and antibodies to the virus were not detected in her breast milk. No reports have indicated vertical transmission of SARS-CoV, a finding that is supported by our data. However, too few cases have been studied to clearly define the risks and provide guidance for treating pregnant women infected with SARS CoV.
OUTPUT:
| PMC3320293 |
MultiCaRe_Reasoning96415 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 7.0
Sex: Male
Title: Right Internal Jugular Vein Phlebectasia: A Rare Cause of Neck Swelling
Keywords: None
Abstract:
Internal jugular vein (IJV) phlebectasia is a rare condition presenting as a self-reducible soft tissue swelling of the neck due to fusiform dilation of the venous wall. We report the case of a 7-year-old boy who presented with painless soft mass in the side of the neck which appears during coughing and straining and reduces spontaneously. Diagnosis was confirmed by Doppler ultrasonography and magnetic resonance imaging of the neck. Conservative management and regular follow-up were considered. In this case report, we highlight this rare benign condition as an uncommon differential of neck swellings in order to avoid unnecessary diagnostic workup and interventions.
Image Caption and Description:
Image caption: Photographs showing appearance of swelling in the neck: (a) when patient is not coughing and (b) when patient is coughing.
Image description: He had 3 x 3 cm, nontender fusiform swelling in the right side of the neck, anterior to the sternocleidomastoid muscle, appearing only at the time of coughing, extending to the anterior triangle of the neck, and the clavicle (Figure 1).
Image caption: Grayscale ultrasound of the neck reveals fusiform dilatation of the right internal jugular vein.
Image description: USG of the neck showed fusiform dilatation of the lower segment of the IJV with a caliber of 2.5 cm, increasing on coughing to 3.1 cm (Figure 2).
Image caption: (a, b) Colour Doppler study of the neck showing uniform colour flow in the dilated internal jugular vein with no thrombosis.
Image description: The Doppler study revealed turbulence in the IJV without any evidence of thrombosis (Figure 3).
Image caption: (a, b, and c) Axial T2-weighted MRI of the neck reveals dilatation of the right internal jugular vein.
Image description: MRI of the neck demonstrated fusiform dilatation of the lower segment of the IJV, increasing in size during coughing (Figure 4).
Case Report:
A 7-year-old otherwise healthy boy presented to outpatient department with a complaint of a painless lump appearing on the right side of the neck while coughing, noticed for the past 3 days. It was not associated with fever, coryza, dyspnea, dysphagia, dysphonia, or facial congestion. There was no history of pain or antecedent trauma or surgery. Family history was unremarkable. On examination, his anthropometric measurements were within the normal range. He had 3 x 3 cm, nontender fusiform swelling in the right side of the neck, anterior to the sternocleidomastoid muscle, appearing only at the time of coughing, extending to the anterior triangle of the neck, and the clavicle (Figure 1). There was no palpable thrill or audible bruit over the swelling. No lymph nodes were palpable in the neck, and oropharyngeal examination was unremarkable. Systemic examination did not reveal any abnormality. USG of the neck showed fusiform dilatation of the lower segment of the IJV with a caliber of 2.5 cm, increasing on coughing to 3.1 cm (Figure 2). The Doppler study revealed turbulence in the IJV without any evidence of thrombosis (Figure 3). MRI of the neck demonstrated fusiform dilatation of the lower segment of the IJV, increasing in size during coughing (Figure 4). Parents were counseled about the benign nature of the condition. Vascular surgery consultation was sought, and conservative management with regular follow-up was planned in view of absence of secondary complications.
OUTPUT:
| PMC5748313 |
MultiCaRe_Reasoning96416 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 73.0
Sex: Female
Title: Spontaneous Remission in an Older Patient with Relapsed FLT3 ITD Mutant AML
Keywords: None
Abstract:
Spontaneous remission (SR) of acute myeloid leukemia (AML) is a very rare phenomenon. AML characterized by FLT3 internal tandem duplication (FLT3 ITD) is typically associated with an aggressive clinical course with rapid progression, relapse, and short overall survival in the absence of transplantation. We report here the first case of SR of FLT3 ITD mutant AML in the literature. Our patient was an elderly woman with relapsed NPM1 and FLT3 ITD mutant AML whose disease underwent SR for a brief duration without precipitating cause. We review the potential immune mechanisms underlying SR in AML and discuss the implications for novel immunotherapeutic approaches for FLT3 mutant AML.
Image Caption and Description:
Image caption: Bone marrow morphology. (a) At time of first detected disease relapse (BM-1); (b) first detection of spontaneous remission (BM-2); (c) second detection of spontaneous remission (BM-3). All marrow aspirate slides were photographed at magnification x1000.
Image description: She underwent screening bone marrow biopsy and aspirate (Figure 1(b)) on the contralateral side from BM-1 approximately one week apart.
Given these incongruent marrow findings, another bone marrow biopsy and aspirate procedure (Figure 1(c)) was performed on the ipsilateral side as BM-1 another week later.
Case Report:
The patient was a 73-year-old woman with a prior medical history of hypertension who presented with three weeks of dyspnea, nausea, loose stools, and fatigue. Examination was unremarkable. However, complete blood count (CBC) revealed leukocytes of 240,000/muL, hemoglobin of 6.2 g/dL, and platelets of 119,000/muL (Table 1). Peripheral smear showed many promonocytes and a few immature blasts containing rare Auer rods consistent with a diagnosis of AML. Emergent leukopheresis and treatment with hydroxyurea were initiated. Bone marrow biopsy and aspirate showed 73% myeloblasts and immature promonocytes expressing CD13, CD15, CD33, CD45, CD64, CD123, and HLA-DR by immunohistochemistry (IHC) and flow cytometry (FC). Cytogenetic analysis showed a normal karyotype. FLT-3 ITD and exon 12 mutation of the nucleophosmin-1 (NPM1) gene were detected (data not shown). Findings were consistent with NPM1-mutated AML of FAB M5 subtype.
Induction chemotherapy with standard-dose cytarabine (100 mg/m2 once daily x 7 days) and daunorubicin (45 mg/m2 once daily x 3 days) was initiated. The patient achieved a complete remission (CR) based on count recovery and repeat bone marrow aspirate showing no blasts or promonocytes. At the time of morphologic CR, no FLT3 mutation was identified by quantitative PCR in the marrow; however, exon 12 mutation of NPM1 was identified in a very small fraction of the cells (signal was below the 10% sensitivity control). Allogeneic stem cell transplantation was offered given the high risk for disease progression, but patient declined. She subsequently received two cycles of high-dose cytarabine (1.5 g/m2 once daily x 6 days), which she tolerated well with complete count recovery.
Six months after completion of consolidation therapy and eight months from her diagnosis, the patient was noted on routine follow-up to have mild leukopenia of 3,300/muL and thrombocytopenia of 115,000/muL. Repeat bone marrow biopsy and aspirate (Figure 1(a)) showed 64% myeloblasts which expressed a slightly different immunophenotype than originally (CD13, CD33, CD15, CD58, CD117, and HLA-DR). Cytogenetics revealed a new abnormality in the form of del (15q) in 19/20 analyzed cells. Both NPM1 and FLT3 ITD mutations were identified with a FLT3 ITD allele/wild-type ratio of 0.36.
The patient was referred to a clinical trial of an experimental FLT3 inhibitor. She underwent screening bone marrow biopsy and aspirate (Figure 1(b)) on the contralateral side from BM-1 approximately one week apart. Surprisingly, this demonstrated cellular marrow with 3% blasts without Auer rods and no evidence of AML by marrow IHC and FC. Cytogenetics revealed del (15q) in 1/20 analyzed cells. Molecular analyses detected the presence of a very small amount of NPM1 mutation in the blood and marrow and a minimal amount of FLT3 with an allelic ratio of 0.005 in the peripheral blood only. The patient reported no interim known or suspected infections or administration of blood products between BM-1 and BM-2. Given these incongruent marrow findings, another bone marrow biopsy and aspirate procedure (Figure 1(c)) was performed on the ipsilateral side as BM-1 another week later. This specimen also showed no evidence of AML by morphology or FC with 2% blasts. Cytogenetics revealed del (15q) in 6/20 analyzed cells. Molecular analyses on marrow aspirate showed detectable NPM1 and FLT3 mutations with a FLT3 ITD allele/wild-type ratio of 0.01. To confirm that these marrow samples were indeed from the same patient, genomic DNA was extracted from the BM-1, BM-2, and BM-3 marrow samples followed by amplification of nine short tandem repeat loci (D3S1358, vWA, FGA, D8S1179, D21S11, D18S51, D5S818, D13S317, and D7S820) using the AmpFLSTR Profiler Plus PCR Amplification Kit from Life Technologies. All of the samples had identical results at all nine loci, thus confirming that the specimens were from the same individual. Unfortunately the patient was not deemed a candidate for clinical trial of experimental FLT3 inhibitor due to the lack of overt morphological disease, which was an eligibility criterion. She elected to resume observant therapy.
Thirty-five days from first documented SR (BM-2), the patient presented with overt disease recurrence with leukocytes of 29,900/muL and 16% peripheral blasts. Marrow biopsy revealed 84% myeloblasts with del (15q) in all 20 analyzed cells and new del (16q) in 1 of 20 cells. Molecular analyses confirmed the same NPM1 and FLT3 ITD mutations with a high allelic ratio of 1.99. The patient decided to forego further treatment and died a few weeks later.
OUTPUT:
| PMC5227128 |
MultiCaRe_Reasoning96417 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 0.0
Sex: Male
Title: A case of bilateral abdominoscrotal hydroceles without communication with the peritoneum
Keywords: abdominoscrotal hydrocele; communication; peritoneum;
Abstract:
Abdominoscrotal hydrocele (ASH) is an uncommon entity. Although various theories on the development of ASH have been proposed, its etiology is still unclear. According to several etiological theories, it is necessary that ASH have communication with the peritoneum. We present a case of bilateral ASH that had no communication with the peritoneum.
Image Caption and Description:
Image caption: T2-weighted magnetic resonance images from the coronal; (a) axial; (b) views. The bilateral massive hydroceles extended into the abdomen through the inguinal canal. Hydrocele; H, Bladder; B, Testis; T
Image description: Magnetic resonance imaging (MRI) confirmed the US findings [Figure 1].
Image caption: Laparoscopic findings in the left; (a) right; (b) sides. No patent processus vaginalis was found on either side. The abdominal cavity was compressed extraperitoneally by the abdominal component of the right abdominoscrotal hydrocele. IR shows the internal inguinal ring
Image description: The abdominal cavity was compressed extraperitoneally by the abdominal component of the right ASH [Figure 2].
Case Report:
A 3-month-old boy was referred with a history of bilateral scrotal hydroceles since birth. On physical examination, large inguinoscrotal hydroceles were noted on both sides. After a 3-month period of observation, ultrasonography (US) showed extension of the bilateral hydroceles through the inguinal canal into the abdomen. Magnetic resonance imaging (MRI) confirmed the US findings [Figure 1]. Surgical repair was scheduled for 2 months later. Laparoscopy was performed through an infraumbilical incision before hydrocelectomies. No patent processus vaginalis was found on either side. The abdominal cavity was compressed extraperitoneally by the abdominal component of the right ASH [Figure 2]. Subsequently, bilateral hydrocelectomies were performed through bilateral inguinal incisions. The procedure was difficult because of adherence of the hydroceles to the spermatic cord. No obvious communication between the peritoneum and the hydrocele was found on either side. Only thin connective tissues were observed. The abdominal portion of the ASH was completely resected, whereas the inguinoscrotal portion was reduced with particular attention to the spermatic vessels and vas deferens. Bilateral high ligations of the peritoneum at the internal inguinal ring (IR) were added to prevent inguinal hernias because the IRs were enlarged by the hydroceles. The patient has been doing well postoperatively without evidence of recurrence.
OUTPUT:
| PMC2878427 |
MultiCaRe_Reasoning96418 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 66.0
Sex: Female
Title: Vanishing bone metastases: a pitfall in contrast-enhanced CT in patients with venous thrombosis
Keywords: None
Abstract:
Enhancement patterns of visceral venous collaterals are well documented in cases of superior vena cava obstruction. Only recently has intraosseous venous collateral enhancement been described. We describe an unusual case of vertebral marrow enhancement in the lower thoracic spine related to venous collateral circulation caused by an incidental hemiazygos thrombus. Misinterpretation of this finding can lead to the erroneous interpretation of sclerotic bone metastases.
Image Caption and Description:
Image caption: (a-d) A 66-year-old female with a history of lung and breast cancer presents with new onset abdominal pain. Contrast-enhanced CT scan of the abdomen and pelvis (a-c) reveals abnormal high attenuation within the lower thoracic vertebrae. Comparison was made with a prior study performed in 2011 (d), which showed no bone abnormality at that time. This was interpreted as new osseous metastatic disease.
Image description: T11 and T12 vertebral bodies and posterior elements (Figure 1). This was initially attributed to recurrence of disease with new osseous involvement.
Image caption: (a-d) Non-contrast positron emission tomography CT centred at the site of previous abnormal vertebral body attenuation demonstrates no 18-fludeoxyglucose-avid metastatic disease with the abnormal attenuation in question no longer apparent (a). Review of the prior contrast-enhanced CT scan in question (b-d) revealed subtle thrombus in the hemiazygos vein (arrow) with much of the abnormal attenuation centred in the basivertebral veins (c). On delayed phase, the abnormal attenuation has resolved (d).
Image description: Careful review near the source of marrow enhancement revealed incidental thrombus in the hemiazygos vein (Figure 2).
Case Report:
A 66-year-old female with a history of breast and lung cancer, both treated and in remission, presented with new onset of generalized abdominal pain. Physical examination and laboratory work-up were unrevealing as to a potential cause.
A contrast-enhanced CT (CECT) of the abdomen and pelvis was performed with series obtained in both arterial and delayed phases that failed to reveal an abdominal or pelvic source of the pain. Comparison with a CECT performed 2 years prior, however, revealed new areas of high attenuation in the T11 and T12 vertebral bodies and posterior elements (Figure 1). This was initially attributed to recurrence of disease with new osseous involvement.
Given the potential of tumour recurrence, a positron emission tomography CT scan was performed without contrast to evaluate the lesion and to assess for other sites of disease. The study revealed normal-appearing thoracic vertebrae without evidence of 18-fludeoxyglucose-avid metastatic disease. On review of the prior CECT in question, it was noted that the majority of the high density areas were centred in the region of the basivertebral veins. In retrospect, this finding was present on arterial phase images and absent on the delayed phase images that prompted a search for the potential cause of this atypical enhancement pattern. Careful review near the source of marrow enhancement revealed incidental thrombus in the hemiazygos vein (Figure 2). It was concluded that thrombus in the hemiazygos vein had caused retrograde opacification of the vertebral venous plexus and its anastomotic capillary sites, which mimicked sclerotic bone metastases.
OUTPUT:
| PMC6180826 |
MultiCaRe_Reasoning96419 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 51.0
Sex: Female
Title: Acute mesenteric ischemia: a sequela of abdominal aortography
Keywords: angiography and transcatheter embolization; aortography; colitis; ischemic; mesenteric artery ischemia;
Abstract:
The use of abdominal angiography and transcatheter embolization has increased rapidly in the last few decades. Although improvement in angiographic techniques has made the procedure safe, ischemic colitis is a rare but potentially dreadful complication. We report a case of a 51-year-old woman who developed ischemic colitis following aortography, demonstrating that such angiographic studies may produce substantial morbidity.
Image Caption and Description:
Image caption: Computed tomography scan of the abdomen (axial view) showing thickening of the colon wall (short thick arrow, on the left) as well as right kidney mass (long thin arrow).
Image description: A CT of the abdomen and pelvis showed thickening of a long segment of colon spanning the distal transverse to the proximal sigmoid colon (Fig. 1).
Image caption: Colonoscopic picture of splenic flexure showing edematous, erythematous, and friable mucosa.
Image description: A colonoscopy showed edematous, erythematous, and friable mucosa overlying the splenic flexure (Fig. 2).
Image caption: Low-power photomicrograph (hematoxylin and eosin stain) of a biopsy of splenic flexure showing focal glandular dropout, small glands with mucin depletion, denudation of surface epithelium, stromal hemorrhage, and fibrosis.
Image description: Biopsy of the affected area showed focal glandular dropout, small glands with mucin depletion, denudation of surface epithelium, stromal hemorrhage, and fibrosis, thus confirming a diagnosis of ischemic colitis (Fig. 3).
Case Report:
A 51-year-old postmenopausal woman, admitted to hospital for a 2-week history of subacute right flank pain, was found to have right renal angiomyolipoma on computed tomography (CT) of the abdomen and pelvis. Past medical history was significant for hypertension treated with lisinopril, allergic rhinitis, and osteoarthritis. She did not smoke or drink alcohol. A percutaneous transfemoral abdominal aortography was performed using ioversol (non-ionic iodinated contrast) for prophylactic embolization of the artery supplying the angiomyolipoma so as to prevent bleeding complications. Selective angiography was performed in multiple projections including the origin of the right renal artery and infrarenal abdominal aorta to study the lower pole of the right kidney where the angiomyolipoma was located. However, embolization could not be performed owing to the inability to isolate a feeding vessel to the tumor. Twelve hours after the procedure, the patient complained of progressively worsening diffuse abdominal pain and bright red rectal bleeding.
On examination, she had a blood pressure of 117/63 mm Hg, heart rate of 94/min, respiration of 16/min, and temperature of 98.1 F. Abdominal examination revealed normal bowel sounds, soft abdomen without any distention, and tenderness over the periumbilical region and left upper quadrant. There was no rebound tenderness. Digital rectal examination showed stool mixed with bright red blood but no hemorrhoids or mass. The remainder of the examination was unremarkable. Laboratory studies included: white blood cell 10,600/mul with 80% granulocytes, hemoglobin 14.4 g/dl, and platelet count 232,000/mul. The glucose, lactate, amylase, lipase, coagulation profile, and liver and renal function tests were all within normal limits.
She was given nil-by-mouth and started on normal saline infusion, intravenous metronidazole, ciprofloxacin, and morphine as needed. She continued to have abdominal pain and multiple bloody bowel movements over the next 2 days. A CT of the abdomen and pelvis showed thickening of a long segment of colon spanning the distal transverse to the proximal sigmoid colon (Fig. 1). A colonoscopy showed edematous, erythematous, and friable mucosa overlying the splenic flexure (Fig. 2). Biopsy of the affected area showed focal glandular dropout, small glands with mucin depletion, denudation of surface epithelium, stromal hemorrhage, and fibrosis, thus confirming a diagnosis of ischemic colitis (Fig. 3). She remained hemodynamically stable throughout the course of her illness and continued to improve over the subsequent 4-5 days. She was discharged on the tenth hospital day.
OUTPUT:
| PMC3937567 |
MultiCaRe_Reasoning96420 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 46.0
Sex: Female
Title: Case Report: Pericardial Effusion Treated With Pericardiectomy Plus Right Atrial Mass Resection: A 2-Year Follow-Up of Cardiac Rosai-Dorfman Disease
Keywords: rosai-dorfman disease; case report; pericardial effusion; pericardiectomy; right atrial mass;
Abstract:
Background: Rosai-Dorfman disease (RDD) is rare a sinus histiocytosis typically causing lymphadenopathy. Heart involvement is anecdotal, and <30 cases of cardiac RDD (cRDD) have been reported so far. Case Presentation: A 46-year old woman with positive clinical history for RDD was admitted to our cardiology department with transthoracic echocardiography diagnosis of severe pericardial effusion and right atrial masses. Pericardiocentesis with catheter insertion was performed 3 days after the admission due to clinical evidence of cardiac tamponade. After 10 weeks of maximal medical therapy for inflammatory pericarditis, including non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, steroids, and anakinra, at least 100 ml of pericardial citric liquid has been daily drained suggesting no clinical improvement. Pericardial liquid analysis demonstrated no malignant cells, but immunohistochemical analysis resulted positive for AE1-AE3, D2-40, S100, and CD68 consistent with an RDD diagnosis. Surgical management was judged clinically indicated, and 2 months after admission, the patient underwent pericardiectomy and debulking of atrial mass with freezing of remaining atrial neoformation. Regular clinical and echocardiography evaluation was performed without pericardial effusion recurrence after 2 years of follow-up. Conclusions: This is the first case ever reported of cRDD who survived after 2 years of follow-up. Pericardiectomy could be feasible and effective for recurrent pericardial effusion in cRDD. Close follow-up and a multidisciplinary environment is needed to take care of cRDD patients.
Image Caption and Description:
Image caption: The timeline of the patient's clinical history is presented.
Image description: A 46-year old woman with positive clinical history for RDD with cutaneous involvement and arthritis, diagnosed 5 years before, was admitted to our cardiology department after transthoracic echocardiography diagnosis of severe pericardial effusion and right atrial masses (Figure 1).
Image caption: Cardiac MRI at presentation showed severe pericardial effusion with mild aortic regurgitation (A), right atrial masses with LGE (B), and mass infiltration of the superior cava vein causing stenosis [red arrow-heads in (C)]. After 1 year of follow-up, cardiac MRI showed no pericardial effusion with moderate mitro-aortic regurgitation (D) and mild increase in right atrial masses' size (E), but with no superior cava vein stenosis [red arrow-heads in (F)].
Image description: Overall, taking into consideration the positive medical history for RDD, cardiac MRI findings were consistent with cardiac involvement of RDD [; Figure 2].
At follow-up, cardiac MRI confirmed the absence of pericardial effusion, the mild and slow progression of atrial masses in the presence of moderate-to-severe mitral regurgitation, and mild-to-moderate aortic regurgitation that was not present at the time of surgery and is possibly related to heart valve involvement of cRDD (Figure 2).
Image caption: Intraoperative view of residual mass freezing (A and Supplementary Video 1) and removal of superior cava vein mass (B and Supplementary Video 2). In (C), gross surgical pathology of the removed mass (7 cm length) is shown, while in (D), infiltrated pericardium is shown after pericardiectomy.
Image description: Surgical management of recurrent pericardial effusion was judged clinically indicated, and 2 months after admission, the patient underwent pericardiectomy and debulking of atrial mass with freezing of remaining atrial neoformation (Figure 3).
After successful resection, the portion of mass involving the superior caval vein was sent for histological analysis and resulted consistent with RDD (Figures 3, 4).
Image caption: The most prominent histological feature is expansion of the cardiac muscular cells that are filled with histiocytes (A). These characteristically have abundant, often vacuolated cytoplasm, rounded nuclei with coarse chromatin, and a single prominent nucleolus. The atypical histiocytes express CD68 (B). In contrast to reactive sinus histiocytes, they are S100 positive (C) but negative for CD1a (D). All these features are consistent with RDD.
Image description: After successful resection, the portion of mass involving the superior caval vein was sent for histological analysis and resulted consistent with RDD (Figures 3, 4).
Image caption: The identification of emperipolesis, defined as the presence of an intact cell within the cytoplasm of another cell. This finding is reported to be typical of RDD and provides a differential diagnosis with PS100+ Erdheim-Chester disease.
Image description: Emperipolesis was demonstrated as well (Figure 5).
Case Report:
A 46-year old woman with positive clinical history for RDD with cutaneous involvement and arthritis, diagnosed 5 years before, was admitted to our cardiology department after transthoracic echocardiography diagnosis of severe pericardial effusion and right atrial masses (Figure 1). At admission, she referred dyspnea during ordinary activity (NYHA III), but no clinical signs of heart failure were present. Cardiac auscultation demonstrated soft heart sounds but pulsus paradoxus was detectable in the presence of sinus tachycardia and normal arterial pressure values (120/70 mmHg). Blood examination showed leukocytosis (WBC 25,000/mul, n.v. <10,000/ul) and increased inflammatory indexes (CRP 47.5 mg/l, n.v. <7 mg/l), while kidney and liver function indexes as well as BNP and Tn-I values were normal. Cardiac MRI confirmed the presence of severe pericardial effusion without concomitant signs of pericardial inflammation. Three separate right atrial neoformations were identified in the interatrial septum and near the right lateral atrioventricular junction (maximum size 13 x 19 mm involving the lateral wall of the right atrium). These masses appeared solid, with smooth borders, but with atrial wall infiltration; of note, superior cava vein involvement with caliber reduction was evident. Masses had inhomogeneous hyperintense signal at T2-weighted images with post-contrast enhancement (both first-pass perfusion images and late gadolinium enhancement). Overall, taking into consideration the positive medical history for RDD, cardiac MRI findings were consistent with cardiac involvement of RDD [; Figure 2]. Possible differential diagnosis was primarily represented by cardiac metastasis from a primitive oncological disease, taking into consideration that this is the most common category of cardiac tumor, especially if multiple lesions are documented in the presence of pericardial effusion, like in this case. However, a total body positron emission tomography was performed and resulted negative for active oncological lesion.
Due to clinical evidence of cardiac tamponade 3 days after hospital admission, pericardiocentesis with catheter insertion was performed. Pericardial fluid analysis demonstrated no malignant cells, and immunohistochemical analysis showed the presence of histiocytes positive for AE1-AE3, D2-40, S100, and CD68 consistent with an RDD diagnosis.
After a total of 10 weeks of maximal medical therapy for inflammatory pericarditis including non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, steroids, and anakinra according to current clinical guidelines, at least 100 ml of pericardial fluid has been daily drained suggesting no clinical improvement.
Surgical management of recurrent pericardial effusion was judged clinically indicated, and 2 months after admission, the patient underwent pericardiectomy and debulking of atrial mass with freezing of remaining atrial neoformation (Figure 3). In this scenario, although radical resection was not achievable, a debulking approach was indicated to prevent mediastinal syndrome due to complete SVC occlusion; this target, in fact, seemed to be more effectively obtained by surgery rather than radiotherapy. After successful resection, the portion of mass involving the superior caval vein was sent for histological analysis and resulted consistent with RDD (Figures 3, 4). More precisely, the characteristic histiocytes were found with abundant and vacuolated cytoplasm, rounded nuclei with coarse chromatin, and a single prominent nucleolus. Emperipolesis was demonstrated as well (Figure 5). The post-operative course was uneventful, and the patient was dismissed 2 weeks after surgery in good clinical condition. Regular clinical and echocardiography evaluation was performed, and patient had no pericardial effusion. At follow-up, cardiac MRI confirmed the absence of pericardial effusion, the mild and slow progression of atrial masses in the presence of moderate-to-severe mitral regurgitation, and mild-to-moderate aortic regurgitation that was not present at the time of surgery and is possibly related to heart valve involvement of cRDD (Figure 2).
OUTPUT:
| PMC8200491 |
MultiCaRe_Reasoning96421 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 19.0
Sex: Female
Title: Unexpected delivery: a case report of cryptic pregnancy in Nigeria
Keywords: cryptic pregnancy; nigeria; delivery; denial of pregnancy; gestation; neonatal risk;
Abstract:
The etiology of cryptic pregnancy has not been fully elucidated and there exist misconceptions about this phenomenon in our contemporary Nigerian society. This case presents the first case report of cryptic pregnancy in sub-Saharan Africa. A case of a 19 year old overweight female student who presented to the sick bay at 01: 30 hours with a 3-day history of lower back pain, abdominal discomfort and constipation. At the sick bay the general practitioner on call asked if she was pregnant and she vehemently said no, recounting that she sees her menstruation regularly. Abdominal examination however, revealed a gravid uterus of about 36 weeks and vaginal examination showed a fully dilated cervix. She was surprised, terrified and confused and only remembered having unprotected sexual intercourse many months earlier. Barely two hours later, she gave birth via spontaneous vaginal delivery, to a live female infant at 03: 14 hours. This case emphasizes the need for general practitioners and specialists in sub-Saharan Africa to be aware of the phenomenon of cryptic pregnancy, which involves women not being conscious of their gravid state until final weeks of gestation or at delivery, to reduce neonatal and maternal complications.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
A 19 year old overweight female student, Ms K, in Enugu State, South East, Nigeria, who presented to a sick bay at 01: 30 hours with a 3 day history of lower back pain, abdominal discomfort and constipation. Unknown to her, she was in labor. She had reported to the outpatient department of a hospital several months ago with complains of malaise repeatedly overtime; her general practitioner (GP) treated empirically for malaria on each visit with same complaints and the recount that her menstruation was regular. At the sick bay the GP on call asked if she was pregnant and she vehemently said no, recounting that she sees her menstruation regularly. Abdominal examination however, revealed a gravid uterus of about 36 weeks and vaginal examination showed that her cervix was fully dilated. When confronted with the situation, Ms K, was surprised as well as confused. However, she only remembered having unprotected sexual intercourse many months ago. The baby presented in a frank breech position. To facilitate delivery a Pinard maneuver was done. She gave birth via spontaneous vaginal delivery to a live female baby weighing 3 kg at 03: 14 hours. Labor and delivery pain was minimal. Ms K was in absolute shock, she refused to touch the baby, it was dramatic as she struggled to accept that she just became a mother. As a result of the circumstances of the delivery, altered judgement of the mother and the potential neonatal risk; the GP insisted and invited the parents. Her parents arrived at 8: 30 hours, upon sighting the baby they inquired whose it was. They were completely baffled to know the baby was their granddaughter. It was even more difficult for the sudden grandmother, a nurse, who kept wondering how her daughter s gravid state eluded her. Due to the peculiarities of the delivery the GP at the sick bay followed up the case, the baby was christened Peace. The GP asked why the name Peace. Ms K replied "the birth of the baby brought unresolved conflict between her family and the male partner s family". It was after the baby was born that she realized the reason behind all that she had gone through. She had nausea only when she drank cold water, this later stopped. She admitted noticing slight increase in weight and mild abdominal protrusion, this made her do exercises which didn t help. She believes her overweight made her and her relatives not to suspect pregnancy. Ms K was confused as she just couldn t understand what was going on with her body and her GP, who always treated malaria without proper investigation, was of no help either. Ms K said she would have committed suicide if her gravid state was discovered before delivery. When asked why she replied "how on earth was she going to explain her gravid state to her parents".
OUTPUT:
| PMC7490131 |
MultiCaRe_Reasoning96422 | As a physician engaged in clinical diagnostic reasoning, here is a case report from the pubmed, given the title, keywords, abstract and the case report, please analyze the input and accurately identify the diagnosis presented within it.
INPUT: Age: 24.0
Sex: Male
Title: Bell clapper testis, torsion, and detorsion: a case report
Keywords: None
Abstract:
We are presenting a common but interesting case of testicular torsion. Torsion is a common important urological emergency. History and examination is important for diagnosis. Urgent testicular exploration is an important message if in doubt.
Image Caption and Description:
Image caption: []
Image description: []
Case Report:
A 24-year-old male was referred for left groin pain. It was severe and sudden in onset for six to seven hours with no urinary symptoms or urethral discharge. General examination including testicles was normal. He discharged from A&E after reassurance.
He visited emergency department again in 10 days time with left testicular pain. There were no urinary symptoms or history of trauma. Urine and bloods were normal. Diagnosis of epididymo-orchitis was made on clinical as well as radiological findings and he was discharged from hospital. On follow up outpatient visit, left testis was small, high riding, and indurated. An urgent ultrasound confirmed dead testis. He was booked for a left orchidectomy and right orchidopexy.
Few weeks later, he was admitted with right testicular pain and on exploration Bell Clapper testis was found. Right testis was viable and left one was dead. A 3-point fixation of right viable testis and left orchidectomy of dead testis was performed.
OUTPUT:
| PMC3350281 |