They comment on the case of a young woman with symptoms of systemic disease of probable autoimmune origin (lupus) who presents with macrocytic anemia, options 2 and 4 are options to identify the autoimmune disease but what they ask us is what to do to treat the anemia, so we should suspect that the anemia is secondary to the autoimmune disease and therefore request a direct Coombs test, since if it is positive the patient, except in extreme cases, will not be transfused and the primary cause should be treated. It also speaks of rapid onset, which in the case of vitamin B12 is more progressive.

They comment on the case of a young woman with symptoms of systemic disease of probable autoimmune origin (lupus) who presents with macrocytic anemia, [HIDDEN], but what they ask us is what to do to treat the anemia, so we should suspect that the anemia is secondary to the autoimmune disease and therefore request a direct Coombs test, since if it is positive the patient, except in extreme cases, will not be transfused and the primary cause should be treated. It also speaks of rapid onset, which in the case of vitamin B12 is more progressive.

A 26-year-old woman consults for a feeling of generalized weakness that has progressively set in over the course of three weeks, becoming particularly intense in the last two days. For the last couple of years, she reports episodes of joint pain in the hands that have required the use of anti-inflammatory drugs, as well as the appearance of an erythematous lesion of unclear cause in the neckline area, mainly in summer. In the physical examination there was only an evident cutaneous-mucosal pallor and a heart rate of 100 bpm. The hemogram shows: Hb 6 gr/dL, Hto 27 %, MCV 105 fL, 3,420 leukocytes/mm3 (2300 neutrophils/mm3, 800 lymphocytes/mm3, 250 monocytes/mm3, 50 eosinophils/mm3, 20 basophils/mm3), platelets 170,000/mm3. Biochemistry: AST 30 IU/L, ALT 35 IU/L, GGT 59 IU/L, alkaline phosphatase 105 IU/L, LDH 490 IU/L, urea 20 mg/dL, creatinine 0.8 mg/dL. Taking into account the available information, indicate which of the following additional analytical parameters you would need to know in order to make the most appropriate immediate decision:

[A predisposing clinical condition for disseminated tuberculosis: hairy cell leukemia].

Hairy cell leukemia (HCL), a rare and slow-progressive B-cell lymphoproliferative disease, enhances predisposition to infectious complications, especially to disseminated mycobacterial infections. Although the association between HCL and mycobacterial disease has been established, disseminated Mycobacterium tuberculosis infection has been reported only in a few case series. In this report, a disseminated tuberculosis (TB) case who had been diagnosed as HCL with histopathologic examination of the bone marrow after being investigated for the etiology of fever of unknown origin, was presented. A 56-year-old male patient who was admitted to our clinic with the complaints of three weeks' duration fever, chills, night sweats and cough was hospitalized. On physical examination, the body temperature of the patient who appeared very ill, was 39°C. Dispersed macular rash that turned pale when pressure was applied, was detected on the legs, arms and back. There were no signs of peripheral lymphadenopathy, hepatomegaly or splenomegaly. Laboratory results revealed haemoglobin 10 g/dl, white blood cell count 1000/mm3, thrombocytes 143.000/mm3, erythrocyte sedimentation rate 41 mm/h, CRP 200 mg/L, uric acid 9.5 mg/dl, AST 118 IU/L, ALT 102 IU/L and LDH 429 IU/L. Thorax computed tomography showed mediastinal and bilateral hilary lymphadenopathy. Although preliminary diagnosis was lymphoma, examination of acid-fast bacilli in three days sequential sputum samples and sputum culture for the growth of mycobacteria (Bactec MGIT 960 TB system, Becton Dickinson, Md) were performed to rule out miliary TB. Blood cultures were also performed with non-radiometric fully automated TB hemoculture bottles (Bactec TB, Becton Dickinson, Md). Sputum cultures yielded no mycobacterial growth, however M.tuberculosis growth was detected in blood culture on the 27th day of inoculation. Bone marrow biopsy revealed HCL. However the patient died on the 14th day of hospitalization. In conclusion, disseminated tuberculosis should be considered for differentional diagnosis in patients with HCL or similar hematologic malignancies since TB is endemic in Turkey.

[Malignant peritoneal mesothelioma].

The peritoneal mesothelioma is a rare pathology with unspecific symptoms reason to be a difficult diagnosis. We report a case of a 58 year old man with diabetes mellitus type 2, arterial hypertension and smoking; without precedent of asbestos exposure. The patient presented a one month history characterized by progressive increase of the abdominal volume and sensation of fullness; three weeks later they added breathlessness and hyporexia. The patient was in regular general condition; he was not presenting hepatic stigmas, edema or adenomegalies. The examination of thorax and cardiovascular it was normal. The abdomen distended by ascites, not painful, liver and spleen not examined. Laboratory: Hemoglobin 11,9 gr/dl, WBC 6840/mm3 Bands 1 %, lymphocytes 10 %, platelets 620000/mm3, PT 12 seconds, PTT 34 seconds, glucose 158 mg/dl, BUN 20,5 mg/ dl, creatinine 1,2 mg/dl, proteins 6,1 gr/dl, albumin 2,6 gr/dl. LDH 316 U/l, beta2microglobulin 2,2 mg/l (0.83-1.15 mg/l). HBV and HCV negative. Ca 19.9, CEA, AFP and PSA negative. Hemocultive negative. Ascitic fluid: ADA 20,3 U/l, serum-ascitic albumin gradient (SAAG) 1,1. Leukocytes 2237 cells/mm3, PMN 6 %, lymphocytes 90 %, mesothelial cells 4 %, proteins 4,6 gr/dl, albumin 2,34 gr/dl, glucose 44 mg/dl, LDH 1918 U/l. Gram and cultive: negatives. BAAR and cultive: negative . Cytology: mesothelial cells with changes of type reagent, Block cell for tumour cells: negative. Abdominal US: increased peritoneum and abundant ascitic fluid. Thoracic-abdominal CT: left side pleural effusion, severe ascites with thick epyplon. Upper GI endoscopy: moderate gastritis. Colonoscopy: two small sessile polyps in sigmoid colon. The finds of the laparoscopy were interpreted like carcinomatosis or peritoneal tuberculosis. The report of the peritoneal biopsy was informed as suggestive of undifferentiated carcinoma; the reappraisal with inmunohystochemic (calretinin +,cytokeratin +, vimentin +) indicated malignant peritoneal mesothelioma, type epithelial. The evolution was torpid. The patient was transferred to the Service of Oncology where they initiated chemotherapy with Cysplatin (CDDP) and died 20 days later. The malignant mesothelioma peritoneal is a unfrequent entity, with limited therapeutic options; generally detected late, with a palliative treatment.

Ranson criteria

Acute pancreatitis not secondary to gallstones At admission: Blood glucose > 11.11 mmol/L (> 200 mg/dL) Age > 55 years Serum LDH > 350 IU/L Serum AST > 250 IU/L WBC count > 16000 cells/mm3 Within 48 hours: Serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit decreased by > 10% Oxygen (hypoxemia with PaO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L Acute pancreatitis secondary to gallstones At admission: Glucose > 220 mg/dl Age > 70 years LDH > 400 IU/L AST > 250 IU/ 100 ml WBC count > 18000 cells/mm3 Within 48 hours: Serum calcium < 8 mg/dL Hematocrit decreased by > 10% Base deficit > 4 mEq/L BUN increased by > 2 mg/dL Sequestered fluid > 6L

A case of Crimean-Congo haemorrhagic fever with normal laboratory findings.

Crimean-Congo haemorrhagic fever (CCHF) is a tick-borne disease caused by Nairovirus, of the family Bunyaviridae. This is the first case report of a confirmed CCHF case without laboratory abnormality. A 36-year-old woman was admitted to our clinic with the complaints of fever, chills, myalgia and vomiting. She was living in a CCHF-endemic region and had received a tick bite ten days previously. Her complaints had started five days after the tick bite, and bleeding of the nose and vagen followed. Under laboratory analysis, serum white blood cell (WBC) was 7300/mm3, haemoglobin (Hb)11.9 gr/dL, platelet (Plt) count 293000/mm3, aspartate transaminase (AST) was 23 U/L, alanine transaminase (ALT) 14 U/L, lactate dehydrogenase (LDH) 139 U/L, creatinine phosphokinase (CPK) 39 U/L, INR 0.8 and APTT 26.2 seconds. Based on these clinical and epidemiological findings, a diagnosis of CCHF infection was suspected, and the diagnosis of CCHF was confirmed with a blood sample tested by TaqMan-based one-step RT-PCR positivity and IgM antibody positivity. We suggest that patients from an endemic region who have typical epidemiological and clinical findings should be evaluated as a possible case for CCHF even if the laboratory findings are not compatible.

InternalMed_Harrison

Fever ˜38.3° C (101° F) and illness lasting ˜3 weeks and no known immunocompromised state History and physical examination Stop antibiotic treatment and glucocorticoids Obligatory investigations: ESR and CRP, hemoglobin, platelet count, leukocyte count and differential, electrolytes, creatinine, total protein, protein electrophoresis, alkaline phosphatase, AST, ALT, LDH, creatine kinase, antinuclear antibodies, rheumatoid factor, urinalysis, blood cultures (n=3), urine culture, chest x-ray, abdominal ultrasonography, and tuberculin skin test

InternalMed_Harrison

Fever >38.3°C (101°F) on at least two occasions 2. Illness duration of ≥3 weeks 3. 4. Diagnosis that remains uncertain after a thorough history-taking, physical examination, and the following obligatory investigations: determination of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level; platelet count; leukocyte count and differential; measurement of levels of hemoglobin, electrolytes, creatinine, total protein, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, creatine kinase, ferritin, antinuclear antibodies, and rheumatoid factor; protein electrophoresis; urinalysis; blood cultures (n = 3); urine culture; chest x-ray; abdominal ultrasonography; and tuberculin skin test (TST). The range of FUO etiologies has evolved over time as a result of changes in the spectrum of diseases causing FUO, the widespread Percentage of Cases Due to Indicated Cause

Acute pancreatitis

At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11.1 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall >10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L The criteria for point assignment is that a certain breakpoint be met at any time during that 48 hour period, so that in some situations it can be calculated shortly after admission. It is applicable to both gallstone and alcoholic pancreatitis. Alternatively, pancreatitis can be diagnosed by meeting any of the following:[2] Alternative Ranson score Ranson's score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT)

Acute pancreatitis

Practice guidelines state: 2006: "The two tests that are most helpful at admission in distinguishing mild from severe acute pancreatitis are APACHE-II score and serum hematocrit. It is recommended that APACHE-II scores be generated during the first 3 days of hospitalization and thereafter as needed to help in this distinction. It is also recommended that serum hematocrit be obtained at admission, 12 h after admission, and 24 h after admission to help gauge adequacy of fluid resuscitation." 2005: "Immediate assessment should include clinical evaluation, particularly of any cardiovascular, respiratory, and renal compromise, body mass index, chest x ray, and APACHE II score" Ranson score The Ranson score is used to predict the severity of acute pancreatitis. They were introduced in 1974. At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11.1 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours

[Roles of department of laboratory medicine on the new patient clinic].

It is now quite well accepted that laboratory test results are indispensable or of primary significance to accurately diagnose a new patient's disease. Furthermore, most doctors recently find difficulty in appropriately selecting and ordering necessary but not excess laboratory tests and to read and interpret all the given test results correctly. In our hospital the system of the outpatient clinic will be changed basically on a specialty clinic system. In order to operate such a specialty clinic system effectively, it appears quite important to set up a unit to discriminate new unspecified patients properly and to consult them to an appropriate specialty clinic. As a preliminary trial, we opened a new patient clinic in July, 1992. The aim of this clinic is to accurately diagnose the new patients' disease immediately and to send them to the specialty clinic on the day of their first visit. Prior to history taking and physical examination by the attending doctor, the patients are instructed to take a set of laboratory tests. These include urinalysis, chest X-P, ECG, hematological examinations (RBC, WBC, Ht, Hb, PLT and ESR) and biochemical tests (AST, ALT, ALP, gamma GTP, LDH, CPK, Chol, T-Bil, TP, Alb, TG, BUN, Cr, Glu, Na, K, Ca, P and CRP). These results are transferred to the clinic within one hour so that the doctor is able to make the diagnosis effectively and to refer the patients to an appropriate clinic.(ABSTRACT TRUNCATED AT 250 WORDS)

Toxic epidermal necrolysis following combination of methotrexate and trimethoprim-sulfamethoxazole.

A 15-year-old boy with T-cell acute lymphoblastic leukemia (ALL) (FAB L1), diagnosed in 1995, received combination chemotherapy consisting of 6 weeks of induction (vincristine, epirubicin, L-asparaginase, prednisolone) and 2 weeks of consolidation (cytosine arabinosides, etoposide). After achieving remission, for further maintenance of remission, he was treated with 14 cycles of intensive chemotherapy consisting of 6-MP, 10 mg/kg orally on the first 4 days, and cyclophosphamide, 1200 mg/m2, vincristine, 1.5 mg/m2, epirubicin, 15 mg/m2, and cytosine arabinoside, 40 mg/m2, intravenously on days 4, 11, 39, and 40, respectively. On day 18 of each cycle, he received intravenous methotrexate (MTX) infusion in a total dose of 150 mg/m2 plus oral leucovorin (30 mg/m2 ) rescue 36 h after starting MTX therapy. In addition, oral trimethoprim-sulfamethoxazole was given regularly to prevent Pneumocystis carinii infection. The patient achieved remission during the first course of treatment, but 8 months later the disease relapsed. He then received four doses of MTX (800 mg intravenously) plus leucovorin rescue in the following 4 months. During the last MTX therapy, small hemorrhagic bullae were found on the lateral side of the right ankle, but subsided after a few days. Due to partial remission of the disease, he was admitted again in January 1999 for high-dose MTX therapy. An initial hemogram on admission revealed hemoglobin 7.2 g/dL, white cell count 15,200/mm3, platelet count 153/mm3, blood creatinine 0.5 mg/dL, and alanine leucine aminotransferase (ALT) 20 U/L. He received 8500 mg of MTX (5000 mg/m2 ) as a continuous intravenous infusion for 24 h. Thirty-six hours after the start of MTX infusion, leucovorin (30 mg, intravenous) rescue was initiated every 6 h for 3 days. Another preventive measure to cover MTX toxicity included aggressive intravenous fluid replacement (4 L/m2 /day) and the addition of 25 meq/L sodium bicarbonate to the intravenous fluid to alkalinize the urine. Concurrent medication included 6-MP (50 mg) once daily and trimethoprim-sulfamethoxazole (120 mg, 600 mg) twice daily every other day. Plasma MTX levels were 52.36 micromol/L 24 h after MTX infusion, 1.87 micromol/L after 48 h, 0.57 micromol/L after 72 h, and 0.41 micromol/L after 96 h. These indicated delayed MTX plasma clearance. The blood creatinine level was mildly elevated from 0.5 mg/dL to 0.7 mg/dL. Thirty-six hours after the administration of MTX, the patient developed an erythematous painful swelling on the right middle finger. The erythema, with subsequent large bulla formation, progressed to all the fingers, toes, palms, and the soles of the feet. Some erythematous to hemorrhagic papules also appeared on the bilateral elbows. Subsequently, diffuse tender erythema with extensive erosions and focal tiny pustules developed on the back, abdomen, proximal extremities, and face (Fig. 1a,b). A positive Nikolsky's sign was also present. A biopsy specimen of the right dorsal hand lesion revealed parakeratosis, detached acanthotic epidermis with scattered necrotic keratinocytes, dyskeratotic cells and nuclear atypia, neutrophilic exocytosis, and many neutrophils in the papillary dermis (Fig. 2). The skin condition deteriorated rapidly. Toxic epidermal necrolysis-like lesions involved 90% of the total body surface on the fifth day after MTX infusion. Mucositis, diarrhea, involuntary tremor, fever, and chills were noted. The patient was then sent to the burn unit for intensive skin care. Ten days after MTX therapy, profound agranulocytosis and thrombocytopenia (white cell count 100/mm3, platelets 14,000/mm3, and hemoglobin 5.6 g/dL) were found. The patient was then started on granulocyte colony stimulation factor (G-CSF, 5 microg/kg/day), but his general condition deteriorated rapidly and he died 6 days later due to septic shock and multiple organ failure.

[Clinical diagnosis and laboratory data].

Modern medicine can not be practiced without laboratory tests. Laboratory tests play a vital role from the initial stage of clinical examination. The Japanese Society of Clinical Pathology has formed a committee specifically dealing with the effective and economic use of lab tests without missing or duplicating the important tests. As is shown in table 1 in the main text "Essential Laboratory Tests" were initially agreed as those tests a patient should take when visiting a clinic regardless of the complaint. From an early stage, laboratory tests were done simultaneously with history-taking and physical examinations. Then the "Initial Impression" is obtained and "Organ-oriented 1st and 2nd screening tests" and confirmatory tests will be done to make the final diagnosis. To evaluate the validity of the "Essential Laboratory Tests", we performed the tests on 1026 patients who visited our general medicine clinic for the first time. We compared the Initial Impression with or without Essential Laboratory Tests. Cases in which a diagnosis could not be made by history-taking and physical examination were decreased from 17.4% to 8.0% by performing the essential laboratory tests. Diagnoses made without the essential laboratory tests were found to be mistaken in 10.4% and the additional use of the tests was suggested to lead to a more accurate diagnosis. In 110 cases, diseases unrelated to the chief complaints, were discovered. Even for the respiratory tract infection, CRP and WBC count, which were included in the essential laboratory tests, were very informative.

[Leukopenia due to anti-tuberculous chemotherapy including rifampicin and isoniazid].

To examine the incidence rate by age and gender of leukopenia caused by chemotherapy including rifampicin (RFP) and isoniazid (INH), and to study the relationships between the leukopenia and the hepatic side effect or other haematological disorders such as thrombocytopenia. Out of the tuberculosis patients who were admitted to our hospital in 1987-88, 1991-92, and 1996-2000, 1,525 patients (1,153 men, 372 women) were chosen for our study who had the white blood cell counts (WBC) in the peripheral blood more than 3,000/mm3 before chemotherapy, and underwent haematologic examination at least twice within 3 months after starting chemotherapy. The definition of leukopenia was as follows: 1) WBC became less than 3,000/mm3 during chemotherapy for patients with pre-treatment WBC more than 4,000/mm3, or 2) WBC decreased more than 1,000/mm3 in patients with pre-treatment WBC between 3,000 and 4,000/mm3. The incidence rates of leukopenia by age, gender, and regimens of chemotherapy were calculated. The case-control study was done between the control and the leukopenia groups excluding patients suffered from agranulocytosis to clarify the hematological and biochemical characteristics of the leukopenia group. The control patients were chosen in the following way. For each patient with leukopenia, a patient with the same admission year, same gender, same regimen of chemotherapy, and the nearest age was chosen as a control patient. The changes in counts of white blood cell, granulocyte, and platelet, in hemoglobin concentration, and in hepatic enzyme levels before and during chemotherapy were compared between the leukopenia and the control groups. Thrombocytopenia was defined as platelet count less than 15 x 10(4)/mm3 and hepatic dysfunction as either asparate aminotransferase (AST) higher than 31 IU/l or alanine aminotransferase (ALT) higher than 34 IU/l. (1) Incidence rate of leukopenia The leukopenia appeared in 36 patients (14 men, 22 women), two (one man, one woman) of whom showed agranulocytosis. The incidence rate was 1.2% (14/1,153) for men and 5.9% (22/372) for women. The incidence rate of women was higher than that of men in the age groups between 20 to 79 y.o., but no difference was seen in the age groups elder than 80 y.o. There were no differences in the incidence rate among groups treated with HRE (E: ethambutol), HRS (S: streptomycin), and HREZ (Z: pyrazinamide). The chemotherapy was continued in 30 patients after the appearance of leukopenia, and the natural recovery from leukopenia was seen in 19 patients, while the leukopenic state lasted during the chemotherapy in the remaining 11 patients. In two patients who exhibited agranulocytosis all drugs were discontinued. In the remaining 4 patients one or more drugs were discontinued. (2) Case-control study between leukopenia (N = 34) and the control (N = 34) groups There were no differences in age, sputum culture positivity on admission, degree of roentgenographic extent of the disease, ratio of cavity formation, and quantity of daily doses between the two groups. There was also no difference between the days until leukopenia appeared after starting chemotherapy (47.6 +/- 29.5 days) in the leukopenia group, and the days until WBC count became minimum within 3 months after starting chemotherapy (41.7 +/- 21.0 days) in the control group. The negativity of tuberculin skin testing was higher in the leukopenia group [7/14 (50%)] than in the control group [1/10 (10%)], however, the difference was statistically not significant due to rather small size of cases. Before the starting chemotherapy, the counts of WBC (7,230 +/- 1,530 vs 5,500 +/- 1,510/mm3, p < 0.001), neutrophil (5,230 +/- 1,450 vs 4,320 +/- 1,620/mm3, p < 0.05), lymphocyte (1,440 +/- 830 vs 830 +/- 440/mm3, p < 0.001) and platelet (34.9 +/- 12.2 vs 24.1 +/- 6.4 x 10(4)/mm3, p < 0.001) in the peripheral blood and the globulin level (3.71 +/- 0.61 vs 3.35 +/- 0.61 g/dl, p < 0.05) in the serum were significantly higher in the control group than in the leukopenia group. The decrements in the counts of WBC and granulocyte during chemotherapy were larger in the leukopenia group than in the control group (delta WBC: 2,880 +/- 1,530 vs 1,910 +/- 1,520/mm3, and delta Neut: 2,840 +/- 1,510 vs 1,820 +/- 1,380/mm3, p = 0.01, respectively), but the counts of lymphocyte were similar in both groups. The platelet counts also decreased in both groups, but to the mid-normal level in the control group, and to the lowest normal level in the leukopenia group, in which 15 out of 34 patients (44%) showed thrombocytopenia. The levels in the serum of hepatic enzymes such as AST, ALT, and gamma-GTP (gamma-glutamyl aminotransferase) increased during chemotherapy in the leukopenia group, while decreased in the control group, and the facts indicate that in the former not only bone marrow cells but also hepatic cells were impaired by anti-tuberculosis drugs. Leukopenia may occur in the course of treatment with anti-tuberculosis drugs, but it is not necessary to stop the chemotherapy immediately, because the WBC count recovers spontaneously or remains under stable leukopenic state during chemotherapy in most cases. But when leukopenia appears, the peripheral blood counts must be checked cautiously, and the chemotherapy should be stopped if the WBC count progressively decreases. The patients who showed leukopenia due to anti-tuberculosis drugs may have had weaker natural and acquired (cell-mediated) immunologic response to tuberculosis infection, and more vulnerable bone marrow cells and hepatic cells to anti-tuberculosis drugs than the control.

[Laboratory findings in patients with hemorrhagic fever with renal syndrome].

To examine the frequency and distribution of hematologic and biochemical laboratory findings in 94 patients with hemorrhagic fever with renal syndrome (HFRS) in the epidemic year 2002. The following laboratory findings were retrospectively analyzed: erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), hemoglobin, hematocrit, leukocyte count and differential percentage (segmented neutrophils, band neutrophils, atypical lymphocytes), platelet count, coagulation tests, blood urea nitrogen (BUN), creatinine, urine, potassium, bilirubin (BIL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase (GT), alkaline phosphatase (ALP), and serum protein electrophoresis. The study included 94 HFRS patients treated at the Dr Fran Mihaljević University Hospital for Infectious Diseases in Zagreb during 2002. ESR increase, mostly mild to moderate, was found in 86.2% of study patients. Increased CRP was recorded in 98.9% of study patients, however, one-fourth had CRP higher than 100 mg/L. Leukocytosis was recorded in 38.3% (10.1 +/- 4.2 x 10(9)/L), thrombocytopenia in 89.4% patients (68.2 +/- 48.3 x 10(9)/L), and severe thrombocytopenia (x 10(9)/L) in six patients. Three patients had abnormal coagulation tests. Increased values of BUN and creatinine were recorded in more than a half of patients, while only four patients had mild hyperkalemia. Only three patinets required hemodialysis. Mildly to moderately increased values of aminotransferases (AST, ALT, GT) were observed in more than 2/3; hypoalbuminaemia in nearly 1/3, and elevated alpha-2 fraction in more than 2/3 of patients. The majority of patients had pathologic urine findings. First laboratory abnormalities were usually found between day 5 and 7 of the disease (increased CRP level, thrombocytopenia, leukocytosis, and elevation of hemoglobin and hematocrit). Biochemical abnormalities(elevation of cratinine and urea, increased levels of aminotransferases) usually occurred at the beginning of the second week, and ESR increase in the second week of disease. The majority of our patients had laboratory findings characteristic of HFRS. Thrombocytopenia and increased level of CRP were the most common laboratory findings during the first week of the disease. Renal and liver impairment occurred at the beginning of the second week of the disease.

Fulminant hepatic failure due to dengue.

Dengue Fever (DF) is only rarely considered as a cause of acute liver failure even globally and only a few case reports of acute hepatic failure and encephalopathy occurring in DF in adults are available. We report a case of Acute Liver Failure due to Dengue during a major outbreak in 2010 in Chitwan. A 20 year old previously healthy female presented to the emergency department of Chitwan Medical College with fever, jaundice and altered sensorium. She was tested positive for Dengue IgM. Her biochemical and clinical parameters were suggestive of acute liver failure with total billirubin of 10.1 mg/dL, direct billirubin of 5.2 mg/dL, ALT 5760 IU, AST 14100 IU, alkaline phosphatase of 1250 IU, PT INR of 1.76 and platelet count of 30,000/mm3. Other causes for acute hepatic failure like acute viral hepatitis, leptospirosis, malaria, Reyes syndrome were ruled out. The patient was admitted and managed in the ICU with supportive care and platelet transfusion. With treatment she made a significant clinical and biochemical improvement with AST of 105 IU, ALT of 120 IU and platelet count of 150,000/mm3. She was discharged after 11 days of hospital stay.

[Acute pancreatitis and acalculous cholecystitis associated with viral hepatitis A].

We report the case of a 14 year-old male from Lima. He is a student with a history of bronchial asthma since age 4 receives conditional salbutamol, corticosteroids used for asthma attacks (a crisis in 2010, 1 month ago) Refuses surgery or transfusions. He presented with a two weeks for abdominal pain, nausea, fever, and jaundice. Epigastric pain is colicky and radiated back to righ upper quadrant, refers in addition to nausea and fever, for ten days notice jaundice of skin and sclera. On examen he was lucid, with jaundice of skin and mucous membranes. There was no palpable lymph nodes, abdomen with bowel sounds, soft, depressible, liver span of 15cm, positive Murphy, no peritonitis. The laboratory findings showed hemoglobin 13gr, MCV 90, platelets 461.000/mm3, WBC 4320/mm, lymphocytes 1700 (39%). total bilirubin: 8.8, B Direct: 7.6, ALT (alanine aminotransferase): 3016, AST (aspartate aminotransferase): 984, alkaline phosphatase: 250, albumin: 3.34gr%, globulin: 2.8, amylase: 589 (high serum amylase), TP: 17, INR: 1.6, VHA IgM positive. 89 mg glucose, urea 19 mg%, creatinine 0.5 mg Hemoglobin 13gr, MCV 90 Platelet 461000/mm3, WBC 4320/mm, Lymphocytes 1700 (39%). The nuclear magnetic resonance showed hepatomegaly associated with thickening of gallbladder wall without stones up to 11mm inside. No bile duct dilatation, bile duct 4mm, pancreas increased prevalence of body size. Mild splenomegaly and free fluid in the space of Morrison and right flank. Abdominal ultrasound revealed a gallbladder wall thickness (11mm), without stones in his light. Pancreas to increase volume with peripancreatic fluid free perivesicular with a volume of 430 cc. Findings consistent with acute acalculous cholecystitis and acute pancreatitis. CT-scan showed enlarged pancreas with predominance of body and tail with peripancreatic edema; the gallbladder was thickening. We report this case because the extrahepatic manifestations of viral hepatitis A infection are uncommon, specially the associated with acute acalculous cholecystitis and acute pancreatitis simultaneous.

Obstentrics_Williams

Neutrophils (x 103/mm3) 1.4-4.6 3.6-10.1 3.8-12.3 3.9-13.1 4,6,9,42 Lymphocytes (x103/mm3) 0.7-4.6 1.1-3.6 0.9-3.9 1.0-3.6 4,6,9,42 Monocytes (x103/mm3) 0.1-0.7 0.1-1.1 0.1-1.1 0.1-1.4 6,9,42 Eosinophils (x 103/mm3) 0-0.6 0-0.6 0-0.6 0-0.6 6, 9 Basophils (x103/mm3) 0-0.2 0-0.1 0-0.1 0-0.1 6,r9 200-400c 254-344 220-441 288-530 39,r42 Transferrin, saturation 22-46b Not reported 10-44 5-37 Transferrin, saturation 22-46b Not reported 18-92 9-98 Creatinine (mg/dL) 0.5-0.9d 0.4-0.7 0.4-0.8 0.4-0.9 39,r42,r45 Gamma-glutamyl 9-58 2-23 4-22 3-26 5,r42,r39,r70 transpeptidase (GGT) Lactate dehydrogenase 115-221 78-433 80-447 82-524 42,29,39,r70 Magnesium (mg/dL) 1.5-2.3 1r.6-2.2 1.5-2.2 1.1r-2.2 3,r26,r29,r39,r42,r48,r63 Osmolality (mOsm/kg H2O) 275-295 275-280 276-289 278-280 17,r63 Phosphate (mg/dL) 2.5-4.3 3.1r-4.6 2.5-4.6 2.8-4.6 3,r26,r33,r39,r42 Potassium (mEq/L) 3.5-5.0 3.6-5.0 3.3-5.0 3.3-5.1 20,r26,r29,r39,r42,r63,r66

Diagnostic peritoneal lavage

Procedure After the application of local anesthesia, a vertical skin incision is made one third of the distance from the umbilicus to the pubic symphysis. The linea alba is divided and the peritoneum entered after it has been picked up to prevent bowel perforation. A catheter is inserted towards the pelvis and aspiration of material attempted using a syringe. If no blood is aspirated, 1 litre of warm 0.9% saline is infused and after a few (usually 5) minutes this is drained and sent for analysis. Interpretation of results If any of the following are found then the DPL is positive and operative exploration is warranted: 10 cc/blood 100,000 RBCs/mm3 500 WBCs/mm3 Presence of bile, bacteria or food particle Amylase level > 175 IU/mL Bilirubin level > 0.01 mg/dL ALP > 2 IU/L See also Peritoneal washing References Bibliography External links Trauma Man: Images of DPL being performed on a simulator Digestive system procedures Trauma surgery

[Let's interpret laboratory data as physical findings].

It is an important role of a clinical laboratory to provide accurate results of examinations promptly when a physician requires them, and this may be generally achieved. What more can technologists do to improve the medical service? It is more helpful for other medical staff to report crude laboratory data with adequate comments, which can be easily and promptly used in medical treatment. In this reversed clinicopathological conference, the admission periods of patients were divided into several phases: the admission day, from the 1st to 7th days, and from the 1st to 15th days. We closely analyzed routine laboratory data in each phase, and commented on what might be useful for the medical staff to the grasp the pathological state of patients in each phase. If comments from the laboratory become commonly acceptable, clinical laboratories will come to play a more valuable role in medical practice.

[A case of elderly-onset systemic lupus erythematosus (SLE) complicated with severe liver dysfunction and pancytopenia due to myelofibrosis].

A 67-year-old woman was admitted to our hospital with a fever. She had been experiencing arthralgia for about one month. On admission, she had a fever of 38.5 degrees C, was anemic and was experiencing tenderness in the joints of both hands, elbows and feet. Laboratory data revealed proteinuria, urinary cylinders, pancytopenia (WBC 900/mm3, Hb 9.5 g/dl, Plt 7.8 x 10(4)/mm3), liver dysfunction (GOT 414 IU/l, GPT 140 IU/l), and hyper-gamma globulinemia. Antibiotics and granulocyte-colony stimulating factor were administered intravenously. Bone marrow aspiration was unsuccessful, but a bone marrow biopsy revealed bone marrow fibrosis. Immunological examinations were positive for antinuclear antibodies, anti-deoxyribonucleic acid (DNA) antibodies, anti-double stranded anti- DNA antibodies, as well as a decreased level of serum complement and an increased level of serum immune complexes. Tests for viral antigens and antibodies known to cause hepatitis were negative. Based on these findings, a diagnosis of SLE accompanied by liver dysfunction and bone marrow fibrosis was made. Steroid pulse therapy was initiated, but her liver function deteriorated on the first day of steroid therapy, and she died three days later. SLE accompanied by myelofibrosis is extremely rare, and only 17 and cases have been reported to date. Among these reports, the present case is the second oldest subject and the first SLE patient to suffer from both myelofibrosis and severe liver dysfunction.

InternalMed_Harrison

Myocarditis appears to be common in both forms of relapsing fever and accounts for some deaths. Most commonly, myocarditis is evidenced by gallops on cardiac auscultation, a prolonged QTc interval, and cardiomegaly and pulmonary edema on chest radiography. General laboratory studies are not specific. Mild to moderate normocytic anemia is common, but frank hemolysis and hemoglobinuria do not develop. Leukocyte counts are usually in the normal range or only slightly elevated, and leukopenia can occur during the crisis. Platelet counts can fall below 50,000/µL. Laboratory evidence of hepatitis can be found, with elevated serum concentrations of unconjugated bilirubin and aminotransferases; the prothrombin and partial thromboplastin times may be moderately prolonged.

[Undifferentiated connective tissue syndromes (UCTS) accompanied by laryngeal involvement and autoimmune hepatitis].

Here we report a patient with undifferentiated connective tissue syndromes (UCTS) who developed hoarseness during exacerbation of autoimmune hepatitis. A 51-year-old woman was hospitalized in November 1993 because of hoarseness and liver dysfunction. She had demonstrated Raynaud's phenomenon, polyarthralgia and hoarseness since 1992. In August 1993, liver dysfunction was noted. On admission, laboratory data showed mild leukopenia, thrombocytopenia (WBC 3,900/mm3, platelet 12.4 x 10(4)/mm3), and elevations of transaminase (GOT 96 IU/l, GPT 79 IU/l) and IgG (4,556 mg/dl). Anti-nuclear antibody (ANA) and anti-smooth muscle antibody were positive. Other autoantibodies including anti-DNA antibody, anti-Scl 70 antibody were all negative. LE test and LE cells were also negative. On laryngoscopic examination, lesions that appeared similar to a bamboo-joint were noted at the middle of the bilateral vocal cords. Pathological findings of liver biopsy specimen were compatible with autoimmune hepatitis. She was treated with 30 mg of prednisolone. Polyarthralgia, hoarseness and the abnormalities of the transaminase levels improved rapidly. Laryngoscopic findings were also normalized. We considered this laryngeal involvement to be acute laryngitis accompanied by some UCTS, including a typical systemic lupus erythematosus (SLE) because of arthritis, cytopenia and ANA positivity. Involvement of the larynx in collagen disease is rarely mentioned in published reports.

[Evaluation of the quality of diagnostic examinations in ambulatory patients].

100 medical records of male and female patients seen for the first time in 1972 at the Medical Outpatients Department, University of Basel (Switzerland) were reviewed retrospectively to assess the quality of history and clinical as well as laboratory diagnostic procedures. In addition, 10 patients were selected for total re-evaluation by renewal clinical and laboratory examinations. On the basis of entries made in the medical records (format DIN A5) the medical history and the clinical examination were judged to be of good quality. A minimal program for laboratory investigation (sedimentation rate, hemoglobin, leukocyte count, serum-transaminase, BUN, urine for sugar and albumin and urine sediment) and small format chest-X-ray had been carried out according to the rules and supplement by additional investigations in 87%. The retrospective check on 10 patients showed that the first examination had been well done and without omissions. Continuous checking of diagnostic procedures was recognized as important, and changes in the forms used were admitted to be necessary for improving quality.

[Ordering laboratory tests: their quantity and causes of variations among physicians].

To establish whether some physicians contribute more than others to the alarming increase in laboratory related expenditure, 317 consecutive medical files established by 10 residents of an outpatient clinic were analyzed. The expense incurred in establishing a diagnosis varied, according to the physicians involved, by a factor of 4.9 for back pain and 2.6 for acute respiratory illness. The difference is even more striking when the various types of investigation are analyzed (blood count, ESR, X-rays). It is therefore possible to group physicians according to their individual tendency to order tests. This classification is not related to age, sex, former professional experience or sub-specialty in internal medicine. There is a significant correlation (Spearman's test) between this classification and the approach to medicine, as evidenced by analysis of the content of an interview on medical practice. These interviews were conducted double blind, recorded and transcribed to determine psychological traits. Physicians who order a large number of tests are characterized by a high index of uncertainty, as evidenced by the large number of hesitant expressions and a tendency to cut the interview short, showing off to compensate for lack of self-assurance, depersonalized reference to patients, few references to the interviewer, difficulty in establishing a true dialogue. These characteristics can be considered to form a coherent entity which shows that even the material aspects of medical practice are strongly influenced by the physician-patient relationship.

Successful treatment of massive ascites due to lupus peritonitis with hydroxychloroquine in old- onset lupus erythematosus.

Systemic lupus erythematous (SLE) is an auto-immune disease with multiple organ involvements that occurs mainly in young women. Literature data suggest that serositis is more frequent in late-onset SLE. However, peritoneal serositis with massive ascites is an extremely rare manifestation. We report a case of old-onset lupus peritonitis treated successfully by Hydroxychloroquine. A 77-year-old Tunisian woman was hospitalized because of massive painful ascites. Her family history did not include any autoimmune disease. She was explored 4 years prior to admission for exudative pleuritis of the right lung without any established diagnosis. Physical examination showed only massive ascites. Laboratory investigations showed leucopenia: 3100/mm3, lymphopenia: 840/mm3 and trace protein (0.03 g/24 h). Ascitic fluid contained 170 cells mm(3) (67% lymphocytes), 46 g/L protein, but no malignant cells. The main etiologies of exudative ascites were excluded. She had markedly elevated anti-nuclear antibody (ANA) titer of 1/1600 and a significantly elevated titer of antibody to double-stranded DNA (83 IU/mL) with hypo-complementemia (C3 levl was at 67 mg/dL). Antibody against the Smith antigen was also positive. Relying on these findings, the patient was diagnosed with SLE and treated with Hydroxychloroquine 200 mg daily in combination with diuretics. One month later, there was no detectable ascitic fluid and no pleural effusions. Five months later she remained free from symptoms while continuing to take chloroquine. This case was characterized by old age of onset of SLE, the extremely rare initial presentation with lupus peritonitis and massive painful ascites with dramatic response to only hydroxychloroquine treatment.

[Effects of written intervention on the number of laboratory studies per patient].

In the context of economic measures in health care we followed over a period of nine months the consequences of a written intervention on the attitude of house staff to prescribe laboratory tests. Since it is well known that these tests have a major impact on health costs several studies have been conducted to test whether costs can be reduced without sacrifice of treatment quality. The study was undertaken in 1997. It had three phases of three months duration each: one for observation, one with the intervention and a follow-up phase. The laboratory tests requested by eleven physicians for their patients during the first month after the initial visit were analyzed. During the intervention--phase six physicians chosen at random were informed about their own average as well as that of the entire group (mean of the entire observation period of all physicians). Unexpectedly the hypothesis that the number of laboratory tests requested per patient would drop only in the group of informed physicians and should stay the same for the physicians without this intervention did not materialize. The number of performed tests dropped in both groups.

Disseminated Histoplasmosis in an Indonesian HIV-Positive Patient: A Case Diagnosed by Fine Needle Aspiration Cytology.

A 30-year-old Javanese-Indonesian man was admitted with complaints of 3 months persistent fever, weight loss, and fatigue. He had never known his past history of unprotected HIV until the admission. His only risk factor is unsafe sex. The patient seemed well nourished. Physical examination revealed blood pressure 100/60 mmHg, pulse 100 beats per minute, respiratory rate 20 times per minute, and temperature 38.8°C. Multiple cervical and inguinal lymphadenopathies were also found. Electrocardiogram showed anterolateral ischemic finding, whereas chest X-ray were normal. Laboratory test results revealed pancytopenia with hemoglobin of 8.2 g/dL, leucocyte count 2000 cells/mm3, platelet 78000 cells/mm3, hematocrit 25.8%, AST 162 IU/L, ALT 81 IU/L, decreased albumin of 2.72 g/dL. The clinical differential diagnosis were lymphoma or tuberculosis lymphadenopathy.

[Check up of breast cancer stages 1 and 2].

We have studied the efficacy of investigations during follow-up of 430 operable node positive and node negative breast cancer patients. Median follow-up was eight years, and 128 patients had relapsed, 91 with metastatic disease. Eight blood analyses, chest X-ray, limited skeletal X-ray and bone scan examinations were undertaken at regular intervals. Of the patients who had relapsed, 59% had symptoms, 23% were detected by clinical examination and 18% were detected by blood analysis only. X-rays and scintigrams were of little value in proportion to the costs. The combination of three blood analyses was useful. An increase in sedimentation rate (ESR) of more than 10 mm/h, an increase in gamma-glutamyltransferase (GT) of 20 U/l and an increase in alkaline phosphatase (ALP) of 60 U/l or more. By using ESR, gamma-GT, ALP, history and clinical examination, costs could be reduced by 90% while maintaining adequate baseline screening for relapse.

[Comparison of symptoms and clinical and laboratory findings in the first and last weeks of typhoid fever].

In this study we examined the clinical and laboratory findings of 80 in-patients. There is an important difference between sexes (p greater than 0.05). Comparison of ages showed that 7-30 age is more vulnerable than the older group. We found clinical symptoms of fever, chills, headache, abdominal pain, disturbances in bowel function, nausea, vomiting, anorexia, and lassitude in the first two weeks more frequently when compared with the 3rd, 4th, 5th weeks of illness (p less than 0.001). Where physical finding of rose spots, discordant pulse rate are important in the first two weeks (p less than 0.001). Abdominal discomfort is an important symptom both in the first two and in the last three weeks (% 40.3 and % 36 respectively). Hepatomegaly and splenomegaly, were found more frequently in the last three weeks. According to laboratory findings of anemia, leukopenia, increased erythrocyte sedimentation rate and positive blood and feces cultures there is no important difference between the first two and last three weeks (p greater than 0.05). Increase in polynuclear leucocytes is important for the first two weeks, and increase in lymphocytes is important in the last three weeks (p less than 0.001). Positivity of group agglutination tests is 57%, in the first two weeks and 83% in the last three weeks. This difference is found to be important.

[Rhabdomyolysis as the presentation form of COVID-19 infection. Report of one case].

COVID-19 infection causes a systemic inflammatory response, which mainly presents as a febrile syndrome with respiratory involvement. We report a 37-year-old male who consulted for myalgia, nausea and epigastric pain lasting three days. On admission, he had crepitations at the lung bases. The initial laboratory showed a creatine kinase of 62,768 U/L, a LDH of 1,110 IU/L, a creatinine a 2.1 mg/dL, an aspartate aminotransferase of 1,347 IU/L, a D-dimer of 1,140 ng/mL, a ferritin of 1,201 ng/mL and a lymphocyte count of 810 cells/mm3. The chest CT scan was compatible with multifocal pneumonia, suggesting a COVID-19 infection. COVID-19 PCR was positive. The patient was managed with hydration, sodium bicarbonate, ceftriaxone, and azithromycin, with a good clinical response.

Is 'routine' laboratory testing a thing of the past? Current recommendations regarding screening.

A 55-year-old man comes to you for a routine physical examination. He is a nonsmoker who takes no medications and has no signs of acute or chronic disease, and he has not seen a doctor in years. What blood work should you order for this patient? The authors of this article help you answer this question in light of recent advances in technology, restrictions in healthcare reimbursement, and increased sophistication in cost-benefit analysis for laboratory testing.

Blood and urine physiological values in farm-cultured Rana catesbeiana (Anura: Ranidae) in Argentina.

A total of 302 samples of healthy farm-cultured Rana catesbeiana specimens (9-21 months-old, 50-350 g liveweight, 50% each sex) from the north-east of Argentina, were analyzed through spectrophotometry, electrophoresis, densitometry, refractometry and microscopy in order to obtain blood and urine normal values. Confidence intervals (p<0.05) for PCV (28.6-31.6%), RBC (0.40-0.44 T/L), MCV (686-732 fL), hemoglobin (6.41-7.20 g/dL), MCH (151-164 pg), MCHC (22.6-24.0%), WBC (18.7-22.3 G/L), neutrophils (58.4-63.4%), lymphocytes (23.9-29.8%), monocytes (2.1-3.8%), eosinophils (4.6-7.0%), basophils (2.9-4.1%), bleeding time (289-393s), coagulation time (452-696s), prothrombin time (76-128s), urinary density (1.0061-1.0089 g/mL), urinary pH (6,38-6.96)., fibrinogen (0.59-0.99 g/dL), total protein (4.19-4.49 g/dL), albumin (1.49-1.67 g/dL), alpha-1 globulin (0.20-0.24 g/dL), alpha-2 globulin (0.48-0.54 g/dL), beta globulin (0.68-0.77 g/dL), gamma globulin (1.28-1.42 g/dL), albumin/globulin ratio (0.50-0.58), creatinine (4.09-5.56 mg/L). urea (76.1-92.4 mg/L), uric acid (11.5-15.4 mg/L), triglycerides (0.34-0.52 g/L), total cholesterol (0.56-0.67 g/L), HDL-C (0.03-0.05 g/L), LDL-C (0.34-0.44 g/L), alpha lipoprotein (6.01-8.67%). beta lipoprotein (91.3-93.9%), glucose (0.45-0.54 g/L), Na (116-121 meq/L), K (3.42-3.81 meq/L), Cl (100-116 meq/L), Ca (7.98-8.61 mg/dL). P (8.319.36 mg/dL), Mg (2.26-2.55 mg/dL), Fe (105-178 ug/dL), ALP (144-170 [U/L), ALT (10.0-14.8 IU/L), AST (42.8-53.4 IU/L), GGT (7.8-10.6 IU/L), LDH (99-135 IU/L), CHE (151-185 lU/L) and CPK (365-500 IU/L), were obtained. Some parameter ranges were similar to those obtained in amphibians, birds or mammals; others were very different. These parameters are useful to evaluate sanitary, metabolic and nutritional state on captive bullfrogs.

A case of brucellosis presenting with acute hepatitis and bicytopenia.

Although liver involvement is frequently seen in brucellosis, acute hepatitis is a rare clinical entity. In its progress, haematological findings are non-specific and vary in respect to severity. In this paper, we present a case of brucellosis with acute hepatitis and bicytopenia without anaemia. A 19-year-old man presented with a 2-week history of fever, sweating, low back and leg pain, lassitude, loss appetite, nausea and vomiting. He gave a history of raw milk ingestion and animal contact. Physical examination showed signs of icteric skin and sclera, tenderness in the right hypochondriac region and hepatosplenomegaly. On admission to hospital, laboratory tests showed WBC 3500/mmc (polymorphs 63% and lymphocytes 33%), haemoglobin 13.8 g/dL, platelet 89000/mmc, erythrocyte sedimentation rate 19 mm/h, and C-reactive protein 21.7 mg/dL (N<0.8 mg/dL). Biochemical tests were as follows: AST 771 U/L, ALT 471 U/L, ALP 355 U/L, GGT 432 U/L, total bilirubin 2.61 mg/dL, direct bilirubin 1.45 mg/dL and albumin 3.7 g/dL. Viral hepatitis markers were found to be negative (HBsAg, anti-HBc total, anti-HBc IgM, anti-HAV IgM, and anti-HCV). Blood culture grew Brucella melitensis. Leukopenia and thrombocytopenia returned to normal levels at the 7th and 14th day of his admission, respectively. Liver function tests improved at the 28th day. Treatment of the brucellosis was performed with antibiotics (tetracycline 500 mg orally four times daily for 6 weeks and streptomycin 1 g IM once daily for 21 days). Finally, a case of brucellosis with acute hepatitis and bicytopenia was treated with a successful outcome. In conclusion, we suggest that due consideration be taken of bicytopenia/pancytopenia and acute hepatitis in brucellosis cases in Turkey, an endemic region.


In this question there should not be much doubt either (by the way, I think it is more of Pneumology than mine, but well, with this fever my friend Emilienko has deviated), since the clinical picture points to a parapneumonic pleural effusion, the macroscopic characteristics of the fluid seem so and the analysis of it shows us that the effusion is also complicated, almost on the verge of being an empyema (very high LDH, cellularity with predominance of PMN, glucose consumption). In addition, with this pH (and knowing that the effusion is already loculated), the endothoracic tube is more than indicated.

A 64-year-old male presents with fever, cough, dyspnea and right pleuritic pain of 1 week's evolution. Chest X-ray shows a loculated right pleural effusion occupying two thirds of the hemithorax. During thoracentesis, a yellowish fluid is drawn and analysis shows: leukocytes 15,000/uL, 92% neutrophils, glucose 30 mg/dL, pH 7, lactate dehydrogenase 3500 U/L, adenosine deaminase 45 U/L and absence of germs on GRAM stain. What is the most appropriate next course of action in this patient?

Intravenous antibiotic therapy and repeat diagnostic thoracentesis in 24 hours.

Intravenous antibiotic therapy and repeat diagnostic thoracentesis if there is no improvement in 48 hours.

Intravenous antibiotic therapy and evacuative (therapeutic) thoracentesis if any germ is isolated in the pleural fluid culture.

Intravenous antibiotic therapy and placement of a chest tube or catheter to drain all pleural fluid.

Management of parapneumonic effusions.

When a patient with a parapneumonic pleural effusion is first evaluated, a therapeutic thoracentesis should be performed if more than a minimal amount of pleural fluid is present. Fluid obtained at the therapeutic thoracentesis should be gram-stained and cultured and analyzed for glucose, pH, LDH, white blood cells, and differential cell count. If the fluid cannot be drained because of loculations, a chest tube should be inserted and thrombolytic agents administered. If the pleural fluid recurs after the initial therapeutic thoracentesis but the patient is doing well clinically and the initial pleural fluid glucose was greater than 60 mg/dL; the pH, greater than 7.2; the LDH, less than three times the upper normal limit for serum and the cultures are negative; he or she can be observed. If one or more of the aforementioned criteria are not met, a second therapeutic thoracentesis should be performed, with repeat diagnostic evaluations of the pleural fluid. If the fluid recurs a second time, a small chest tube should be placed if the pleural fluid glucose and pH were lower and the LDH higher on the second thoracentesis than on the first thoracentesis. Patients with loculated-parapneumonic effusions should be treated with tube thoracostomy and thrombolytic agents. If drainage is incomplete, thoracoscopy, with breakdown of adhesions and debridement of the pleural space, is indicated. If thoracoscopy is unsuccessful, then thoracotomy, with decortication, is indicated unless the patient is too debilitated.

Explosive pleuritis.

The objective of the present paper is to describe the clinical and computed tomography features of 'explosive pleuritis', an entity first named by Braman and Donat in 1986, and to propose a case definition. A case report of a previously healthy, 45-year-old man admitted to hospital with acute onset pleuritic chest pain is presented. The patient arrived at the emergency room at 15:00 in mild respiratory distress; the initial chest x-ray revealed a small right lower lobe effusion. The subsequent clinical course in hospital was dramatic. Within 18 h of admission, he developed severe respiratory distress with oxygen desaturation to 83% on room air and dullness of the right lung field. A repeat chest x-ray, taken the morning after admission, revealed complete opacification of the right hemithorax. A computed tomography scan of the thorax demonstrated a massive pleural effusion with compression of pulmonary tissue and mediastinal shift. Pleural fluid biochemical analysis revealed the following concentrations: glucose 3.5 mmol/L, lactate dehydrogenase 1550 U/L, protein 56.98 g/L, amylase 68 U/L and white blood cell count 600 cells/mL. The pleural fluid cultures demonstrated light growth of coagulase-negative staphylococcus and viridans streptococcus, and very light growth of Candida albicans. Cytology was negative for malignant cells. Thoracotomy was performed, which demonstrated a loculated parapneumonic effusion that required decortication. The patient responded favourably to the empirical administration of intravenous levofloxacin and ceftriaxone, and conservative surgical methods in the management of the empyema. This report also discusses the patient's rapidly progressing pleural effusion and offers a potential case definition for explosive pleuritis. Explosive pleuritis is a medical emergency defined by the rapid development of a pleural effusion involving more than 90% of the hemithorax over 24 h, which causes compression of pulmonary tissue and mediastinal shift to the contralateral side.

[Parapneumonic pleural effusions and empyema in adults:current practice].

About 20% of hospitalized patients with bacterial pneumonia have an accompanying pleural effusion. Parapneumonic effusions (PPE) are associated with a considerable morbidity and mortality. The main decision in managing a patient with a PPE is whether to insert a chest tube (complicated PPE). Imaging (i.e., chest radiograph, ultrasound and computed tomography) and pleural fluid analysis (i.e., pH, glucose, lactate dehydrogenase, bacterial cults) provide essential information for patient management. Therefore, all PPEs should be aspirated for diagnostic purposes. This may require image-guidance if the effusion is small or heavily loculated. According to the current guidelines, any PPE that fulfills at least one of the following criteria should be drained: size > or = 1/2 of the hemithorax, loculations, pleural fluid pH < 7.20 (or alternatively pleural fluid glucose < 60 mg/dl), positive pleural fluid Gram stain or culture, or purulent appearance. The key components of the treatment of complicated PPE and empyema are the use of appropriate antibiotics, provision of nutritional support, and drainage of the pleural space by one of the following methods: therapeutic thoracentesis, tube thoracostomy, intrapleural fibrinolytics, thoracoscopy with breakdown of adhesions or thoracotomy with decortication. The routine use of intrapleural fibrinolytic therapy remains controversial. (c) 2009 Elsevier España, S.L. All rights reserved.

Pleural effusions caused by infection.

Diagnostic thoracentesis is imperative when pneumonia is accompanied by an effusion (parapneumonic effusion). Examination of the pleural fluid is the only way to differentiate empyema and complicated parapneumonic effusions from uncomplicated parapneumonic effusions, and this differentiation is vital in deciding whether chest tube drainage is needed. If the aspirated pleural fluid contains pus or bacteria, closed chest tube drainage and antibiotic therapy should be started promptly. The same management approach is indicated if the pleural fluid pH is less than 7.00 or the glucose level is less than 40 mg/ml, since these effusions almost invariably are complicated parapneumonic effusions that do not resolve without fluid drainage. If the pleural fluid pH is greater than 7.20 and glucose level is more than 40 mg/ml, antibiotic therapy alone will suffice. Management of parapneumonic effusions with a pH of 7.00 to 7.20 should be based on serial observations of clinical status and pleural fluid findings.

Management of pleural effusions.

This review summarizes current strategies in the treatment of patients with pleural effusion. To determine whether a patient has a transudative or exudative pleural effusion, Light's criteria should be applied to measure the concentrations of protein and lactate dehydrogenase (LDH) in the pleural fluid and serum. If the effusion is transudative, therapy should be directed toward the underlying congestive heart failure, cirrhosis, or nephrosis. Consideration should be given to pleurodesis with a sclerosant if patients with recurrent transudative effusion have severe dyspnea due to their effusion. If the effusion is exudative, attempts should be made to define the etiology. The diagnosis of pleural malignancy is most easily established via pleural fluid cytology. If this is negative and the patient is suspected of having pleural malignancy, thoracoscopy is indicated. The concentrations of adenosine deaminase and gamma-interferon in pleural fluid are useful in the diagnosis of pleural tuberculosis. Patients with pneumonia and pleural effusion should undergo therapeutic thoracentesis; the pleural fluid should be Gram-stained and cultured, and the differential cell count, glucose and LDH concentration, and pH should be determined. Indicators of a poor prognosis include the presence of frank pus, a positive Gram-stain, a pleural glucose concentration of less than 2.2 mmol/L, a pH less than 7.00, the presence of pleural loculations, and an LDH concentration greater than three times the upper limit of normal in serum. If the pleural fluid cannot be completely evacuated because of loculations, intrapleural thrombolytic therapy should be considered. If thrombolytics are ineffective, thoracoscopy or thoracotomy with decortication should be performed. Dyspneic patients with malignant pleural effusions whose dyspnea is relieved with therapeutic thoracentesis should be considered for pleurodesis using a tetracycline derivative. Talc is not recommended because it induces acute respiratory distress syndrome in about 5% of patients, with an overall mortality of 1%.

Parapneumonic effusions and empyema.

Parapneumonic effusions occur in 20 to 40% of patients who are hospitalized with pneumonia. The mortality rate in patients with a parapneumonic effusion is higher than that in patients with pneumonia without a parapneumonic effusion. Some of the excess mortality is due to mismanagement of the parapneumonic effusion. Characteristics of patients that indicate that an invasive procedure will be necessary for its resolution include the following: an effusion occupying more than 50% of the hemithorax or one that is loculated; a positive Gram stain or culture of the pleural fluid; and a purulent pleural fluid that has a pH below 7.20 or a glucose below 60, or has a lactic acid dehydrogenase level of more than three times the upper normal limit for serum. Patients with pneumonia and an effusion of more than minimal size should have a therapeutic thoracentesis. If the fluid cannot be removed with a therapeutic thoracentesis, a chest tube should be inserted and consideration be given to the intrapleural instillation of fibrinolytics. If the loculated effusion persists, the patient should be subjected to video-assisted thoracoscopic surgery, and if the lung cannot be expanded with this procedure, a full thoracotomy with decortication should be performed. The definitive procedure should be performed within 14 d.

Parapneumonic effusions and empyema.

Nearly 50 per cent of patients with acute bacterial pneumonia have an accompanying pleural effusion (parapneumonic effusion). With appropriate antibiotic therapy, the pleural effusion will resolve along with the pneumonia in the majority of patients. However, in a small fraction, the pleural effusion will not resolve unless drainage of the pleural space is instituted. Such patients are said to have complicated parapneumonic effusions. It is important to identify patients with complicated parapneumonic effusions as early as possible, since tube drainage of the pleural space becomes increasingly difficult the longer its institution is delayed. The possibility of a complicated parapneumonic effusion should be considered in every patient with bacterial pneumonia. If both diaphragms cannot be distinctly identified throughout their length on the lateral chest radiograph, decubitus chest radiographs should be obtained. If the thickness of the fluid on the decubitus radiograph is greater than 10 mm, a diagnostic thoracentesis should be performed. Only pleural fluid analysis can identify patients with complicated parapneumonic effusions. Complicated parapneumonic effusions are characterized by low pleural fluid pH and glucose levels, a high pleural fluid LDH, and a positive Gram stain of the pleural fluid. Tube thoracostomy should be performed immediately in a patient with an acute bacterial pneumonia if the pleural fluid glucose is below 40 mg per 100 ml, the pleural fluid pH is below 7.00, or if the Gram stain of the pleural fluid is positive. Patients with pleural fluid pH above 7.20, pleural fluid LDH below 1000 IU per L, and pleural fluid glucose levels above 40 mg per 100 ml respond well to only the administration of appropriate antibiotics.(ABSTRACT TRUNCATED AT 250 WORDS)

Repeated therapeutic thoracentesis to manage complicated parapneumonic effusions.

In complicated parapneumonic effusion (CPPE), antibiotics and evacuation of the infected pleural fluid are mandatory. The first-line evacuation treatment is still controversial. The aim of this article is to highlight the usefulness of repeated therapeutic thoracentesis (RTT) as a first-line treatment. In the most recent study on RTT in CPPE, disposable pleural needles were used and the median number of thoracentesis was 3. The success rate was 81%, and only 4% of the patients were referred for thoracic surgery. The 1-year survival rate was 88%. On multivariate analysis, the observation of microorganisms in the pleural fluid after Gram staining and first thoracentesis volume at least 450 ml was associated with a higher risk of RTT failure. RTT is less invasive and can target different loculated pleural collections. Patients are less confined to beds between each procedure, and could even be ambulatory managed. The use of intrapleural fibrinolytics in association with DNase could most likely enhance the efficacy of RTT. RTT is efficient and well tolerated in the management of CPPE, including pleural empyema, and could be proposed as a first-line therapy for CPPE. This technique could be used in association with intrapleural fibrinolytics and DNase.

Pleural empyema

There is no readily available evidence on the route of administration and duration of antibiotics in patients with pleural empyema. Experts agree that all patients should be hospitalized and treated with antibiotics intravenously. The specific antimicrobial agent should be chosen based on Gram stain and culture, or on local epidemiologic data when these are not available. Anaerobic coverage must be included in all adults, and in children if aspiration is likely. Good pleural fluid and empyema penetration has been reported in adults for penicillins, ceftriaxone, metronidazole, clindamycin, vancomycin, gentamicin and ciprofloxacin. Aminoglycosides should typically be avoided as they have poor penetration into the pleural space. There is no clear consensus on duration of intravenous and oral therapy. Switching to oral antibiotics can be considered upon clinical and objective improvement (adequate drainage and removal of chest tube, declining CRP, temperature normalization). Oral

Thoracic empyema - a review based on three cases reports.

Complicated parapneumonic effusion is one in which an invasive procedure is necessary for its resolution and empyema means pus in the pleural space. An early diagnosis and therapy of these conditions results in less morbidity and mortality. CT of the chest is important to study complex pleural effusions. Loculated effusions, those occupying more than 50% of the thorax, or which show positive Gram stain or bacterial culture, or a purulent effusion with a pH below 7.20, with a glucose level below 60 mg/dl or a LDH level more than three times the upper limit of normal for serum, are indications for an invasive procedure. These characteristics result from the evolution of a not well treated parapneumonic effusion, through the three stages: (1) exsudative; (2) fibrinopurulent; (3) fibrotic. Depending on the stage therapeutic methods vary from therapeutic thoracentesis, insertion of a chest tube with or without instillation of fibrinolytics, video-assisted thoracoscopic surgery, and lung decortication. A review of all these aspects are done based on a series of three cases reports with very different clinical presentation: one patient with empyema by Streptococcus pyogenes and that died rapidly due to massive hemoptysis; a patient with empyema due to acute pneumonia developing during an airflight; a patient with empyema and bacteraemia by Streptococcus pneumonia leading to the diagnosis of an unknown HIV infection.

Pneumonia

Pleural effusion, empyema, and abscess In pneumonia, a collection of fluid may form in the space that surrounds the lung. Occasionally, microorganisms will infect this fluid, causing an empyema. To distinguish an empyema from the more common simple parapneumonic effusion, the fluid may be collected with a needle (thoracentesis), and examined. If this shows evidence of empyema, complete drainage of the fluid is necessary, often requiring a drainage catheter. In severe cases of empyema, surgery may be needed. If the infected fluid is not drained, the infection may persist, because antibiotics do not penetrate well into the pleural cavity. If the fluid is sterile, it must be drained only if it is causing symptoms or remains unresolved.

Pleural effusion

Thoracentesis Once a pleural effusion is diagnosed, its cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis, and it should be done in almost all patients who have pleural fluid that is at least 10 mm in thickness on CT, ultrasonography, or lateral decubitus X-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresis can be tried, and thoracentesis is avoided unless effusions persist for more than 3 days. In a thoracentesis, a needle is inserted through the back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary line, into the pleural space. The use of ultrasound to guide the procedure is now standard of care as it increases accuracy and decreases complications. After removal, the fluid may then be evaluated for:

Serial pleural fluid analysis in a new experimental model of empyema.

Prior attempts to create an animal model of empyema by direct inoculation of bacteria alone into the pleural space have been unsuccessful. The animals either died of overwhelming sepsis or cleared the infection from the pleural space without development of an empyema. We hypothesized that injection of bacteria with a nutrient agar into the pleural space would allow the bacteria to remain in the pleural space for an extended time period, permitting an empyema to develop. The bacterium Pasteurella multocida in brain heart infusion (BHI) agar was injected into the right hemithorax of 12 New Zealand white male rabbits. Our preliminary studies showed that the animals died in less than 7 days if they were not given parenteral antibiotics. For this reason, the rabbits were given penicillin, 200,000 U, IM, every 24 h starting 24 h after bacterial injection. Pleural fluid was sampled by thoracentesis at 12, 24, 48, 72, and 96 h after bacterial injection. Pleural fluid pH, glucose, lactate dehydrogenase (LDH), leukocyte count, and Gram's stain and culture (in one half of the animals) were obtained at each time point. Pleural biopsy specimens were obtained at autopsy after 96 h. The mean pleural fluid pH reached a nadir of 7.01 at 24 h and remained less than 7.1 throughout the experiment. The mean pleural fluid glucose level reached a nadir of 10 mg/dL at 24 h. The mean pleural fluid LDH peaked at 21,000 IU/L at 24 h and the mean pleural fluid leukocyte count peaked at 12 h with a value of 67,000 cells per cubic millimeter. Gram's stains revealed organisms and cultures were positive for growth in all animals at 12 and 24 h. Some animals had positive Gram's stains and growth on cultures up to 72 h after bacterial injection. At autopsy, all rabbits injected with bacteria had gross pus in the right pleural space and had developed a thick pleural peel. Microscopic specimens of the pleura revealed large numbers of leukocytes (primarily polymorphonuclear lymphocytes) with invasion of the adjacent lung and chest wall. In conclusion, this model more closely mimics the empyema that occurs in humans, relative to previous animal models. This model appears appropriate for additional randomized studies in which different methods for the treatment of empyema can be evaluated.

InternalMed_Harrison

2. Pleural fluid pH <7.20 3. Pleural fluid glucose <3.3 mmol/L (<60 mg/dL) 4. Positive Gram stain or culture of the pleural fluid 5. Presence of gross pus in the pleural space If the fluid recurs after the initial therapeutic thoracentesis and if any of these characteristics are present, a repeat thoracentesis should be performed. If the fluid cannot be completely removed with the therapeutic thoracentesis, consideration should be given to inserting a chest tube and instilling the combination of a fibrinolytic agent (e.g., tissue plasminogen activator, 10 mg) and deoxyribonuclease (5 mg) or performing a thoracoscopy with the breakdown of adhesions. Decortication should be considered when these measures are ineffective.

Thoracic Empyema -- Evaluation -- Thoracocentesis

The recommendation is for diagnostic fluid sampling via thoracentesis in all patients with pleural effusions with greater than 2 cm depth on lateral decubitus film or computed tomography, associated with a pneumonic illness, recent chest trauma, surgery or features of ongoing sepsis. [12] [13] Frank pus in the pleural space invariably necessitates surgical drainage. However, if there is uncertainty whether a turbid fluid is infected, a pH less than 7.2 measured via a blood gas analyzer warrants an invasive procedure for drainage. [14] Polymorphonucleocyte predominance, low glucose, and LDH over 1000 on biochemical analysis of pleural fluid support the diagnosis of empyema. Furthermore, fluid culture data should be used to guide appropriate antimicrobial therapy. Research shows that culture yield can be increased significantly if the pleural fluid gets injected into blood culture bottles immediately after aspiration. [15]

Parapneumonic effusion

A parapneumonic effusion is a type of pleural effusion that arises as a result of a pneumonia, lung abscess, or bronchiectasis. There are three types of parapneumonic effusions: uncomplicated effusions, complicated effusions, and empyema. Uncomplicated effusions generally respond well to appropriate antibiotic treatment. Diagnosis The criteria for a complicated parapneumonic effusion include Gram stain–positive or culture-positive pleural fluid, pleural fluid pH <7.20, and pleural fluid LDH that is greater than three times the upper limit of normal of serum LDH. Diagnostic techniques available include plain film chest x-ray, computed tomography (CT), and ultrasound. Ultrasound can be useful in differentiating between empyema and other transudative and exudative effusions due in part to relative echogenicity of different organs such as the liver (often isoechogenic with empyema).

InternalMed_Harrison

The possibility of a parapneumonic effusion should be considered whenever a patient with bacterial pneumonia is initially evaluated. The presence of free pleural fluid can be demonstrated with a lateral decubitus radiograph, computed tomography (CT) of the chest, or ultrasound. If the free fluid separates the lung from the chest wall by >10 mm, a therapeutic thoracentesis should be performed. Factors indicating the likely need for a procedure more invasive than a thoracentesis (in increasing order of importance) include the following: 1. 2. Pleural fluid pH <7.20 3. Pleural fluid glucose <3.3 mmol/L (<60 mg/dL) 4. Positive Gram stain or culture of the pleural fluid 5. Presence of gross pus in the pleural space

Pleural empyema

Treatment Pleural fluid drainage Proven empyema (as defined by the "golden" criteria mentioned earlier) is an indication for prompt chest tube drainage. This has been shown to improve resolution of the infection and shorten hospital admission. Data from a meta-analysis has shown that a pleural fluid pH of <7.2 is the most powerful indicator to predict the need for chest tube drainage in patients with non-purulent, culture negative fluid. Because of the viscous, lumpy nature of infected pleural fluid, in combination with possible septation and loculation, it has been proposed that intrapleural fibrinolytic or mucolytic therapy might improve drainage and therefore might have a positive effect on the clinical outcome. Intrapleural fibrinolysis with urokinase decreased the need for surgery but there is a trend to increased serious side effects.

Asplenia

In an emergency room or hospital setting, appropriate evaluation and treatment for an asplenic febrile patient should include a complete blood count with differential, blood culture with Gram stain, arterial blood gas analysis, chest x-ray, and consideration for lumbar puncture with CSF studies. None of these evaluations should delay the initiation of appropriate broad-spectrum intravenous antibiotics. The Surviving Sepsis Campaign guidelines state that antibiotics should be administered to a patient suspected of sepsis within 1 hour of presentation. Delay in starting antibiotics for any reason is associated with a poor outcome.

Pleural Effusion -- Evaluation

The presence of organisms by gram stain or culture leads to a diagnosis of empyema and necessitates a chest tube for drainage of pus. Cytology is necessary for determining the presence of malignant cells in the pleural fluid. The sensitivity of pleural fluid cytology in the presence of malignant effusion in the first thoracentesis is around 60%, and the yield increases with further attempts, approaching 95% by three samples on different days.  However, if a malignant effusion is strongly suspected and cytology is negative, then medical thoracoscopy with pleural biopsy can be performed after two to three thoracenteses to obtain a diagnosis.

Parapneumonic Pleural Effusions and Empyema Thoracis -- Treatment / Management

Treatment of parapneumonic effusion includes appropriate antibiotic therapy together with drainage of pleural fluid as indicated. Parapneumonic effusion is classified into 4 groups based on risk for the poor outcome: Category 1 (very low risk): The effusion is small (less than 10-mm thickness on decubitus) and free-flowing. No thoracentesis is indicated. Category 2 (low risk): The effusion is small to moderate (equal to 10 mm and less than half the hemithorax) and free-flowing with negative culture and Gram stain regardless of the prior use of antibiotics and pH equal to 7.20. Category 3 (moderate risk), in which one of the following criteria is present: the fluid equal to half the hemithorax, loculated effusion, thicken pleura on contrast-enhanced CT scan, positive Gram stain or culture or pH less than 7.20. Category 4 (high risk): This is when pleural fluid is in the form of pure pus.

Thoracentesis

Tension pneumothorax is a medical emergency that requires emergent needle decompression before a chest tube is placed. Indications This procedure is indicated when unexplained fluid accumulates in the chest cavity outside the lung. In more than 90% of cases analysis of pleural fluid yields clinically useful information. If a large amount of fluid is present, then this procedure can also be used therapeutically to remove that fluid and improve patient comfort and lung function. The most common causes of pleural effusions are cancer, congestive heart failure, pneumonia, and recent surgery. In countries where tuberculosis is common, this is also a common cause of pleural effusions.

Thoracentesis

Cultures and stains If the effusion is caused by infection, microbiological culture may yield the infectious organism responsible for the infection, sometimes before other cultures (e.g. blood cultures and sputum cultures) become positive. A Gram stain may give a rough indication of the causative organism. A Ziehl–Neelsen stain may identify tuberculosis or other mycobacterial diseases. Cytology Cytology is an important tool in identifying effusions due to malignancy. The most common causes for pleural fluid are lung cancer, metastasis from elsewhere and pleural mesothelioma. The latter often presents with an effusion. Normal cytology results do not reliably rule out malignancy, but make the diagnosis more unlikely. References External links A photo gallery of thoracentesis showing the procedure step-by-step. V. Dimov, B. Altaqi, Clinical Notes, 2005. A free PDA version. Medical tests Respiratory system procedures Veterinary diagnosis Interventional radiology 1850 introductions

Surgery_Schwartz

can be avoided in patients with small effusions associated with resolving pneumonia. These patients typically present with cough, fever, leukocytosis, and uni-lateral infiltrate, and the effusion is usually a result of a reactive, parapneumonic process. If the effusion is small and the patient responds to antibiotics, a diagnostic thoracentesis may be unneces-sary. If the effusion is large and compromising respiratory efforts, or if the patient has a persistent white blood cell count despite improving signs of pneumonia, an empyema of the pleural space must be considered. In these patients, early and aggressive drainage with chest tubes is required, possibly with surgical intervention.Once the decision is made to access a pleural effusion, the next step is to determine if a sample of the fluid or complete drainage of the pleural space is desired. This step is influenced by the clinical history, the type and amount of fluid present, the Brunicardi_Ch19_p0661-p0750.indd 73601/03/19

Pleurisy -- Treatment / Management

A category 3 effusion may also be defined as a pH of <7.20 or a positive gram stain/culture (empyema). [13] Category 4 effusions are defined by purulent material on thoracentesis. [13] Category 3 and 4 effusions are recommended to have thoracostomy drainage. [13] Empyema, or category 4 effusions, may require surgical evacuation and decortication. Due to the high mortality of the categories 3 and 4 pleural effusions (30%), additional methods for the complete drainage of the infected pleural fluid include intrapleural fibrinolytic followed by drainage and/or surgical decortication. [14] The MIST 2 trial compared intrapleural placebo, intrapleural DNase, intrapleural tPA, and combination tPA/DNAse in patients with category 3 or 4 effusions.

Pleural empyema

The most often used "golden" criteria for empyema are pleural effusion with macroscopic presence of pus, a positive Gram stain or culture of pleural fluid, or a pleural fluid pH under 7.2 with normal peripheral blood pH. Clinical guidelines for adult patients therefore advocate diagnostic pleural fluid aspiration in patients with pleural effusion in association with sepsis or pneumonic illness. Because pleural effusion in the pediatric population is almost always parapneumonic and the need for chest tube drainage can be made on clinical grounds, British guidelines for the management of pleural infection in children do not recommend diagnostic pleural fluid sampling.

Thoracentesis

The use of ultrasound for needle guidance can minimize the complication rate. Follow-up imaging While chest X-ray has traditionally been performed to assess for pneumothorax following the procedure, it may no longer be necessary to do so in asymptomatic, non-ventilated persons given the widespread use of ultrasound to guide this procedure. Interpretation of pleural fluid analysis Several diagnostic tools are available to determine the etiology of pleural fluid. Transudate versus exudate First the fluid is either transudate or exudate. A transudate is defined as pleural fluid to serum total protein ratio of less than 0.5, pleural fluid to serum LDH ratio > 0.6, and absolute pleural fluid LDH > 200 IU or > 2/3 of the normal.

Pleurisy -- Treatment / Management

Category 2 pleural effusions are >10 mm but less than half of the hemithorax. [13] Category 2 to 4 pleural effusions are recommended to have diagnostic thoracentesis performed, and empyema ruled out (must have negative culture, gram stain, and a pH>7.20).  A category 3 effusion involves more than half of the hemithorax, loculations noted within the pleural space, or thickening of the parietal pleura. [13]

InternalMed_Harrison

P. aeruginosa, or (rarely) S. pneumoniae. Aspiration pneumonia is typically a polymicrobial infection involving both aerobes and anaerobes. A significant pleural effusion should be tapped for both diagnostic and therapeutic purposes. If the fluid has a pH of <7, a glucose level of <2. 2 mmol/L, and a lactate dehydrogenase concentration of >1000 U/L or if bacteria are seen or cultured, then it should be completely drained; a chest tube is often required and video-assisted thoracoscopy may be needed for late treatment or difficult cases.

Pleurisy

Computed tomography (CT) scan A CT scan provides a computer-generated picture of the lungs that can show pockets of fluid. It also may show signs of pneumonia, a lung abscess, or a tumor. Magnetic resonance imaging (MRI) Magnetic resonance imaging (MRI), also called nuclear magnetic resonance (NMR) scanning, uses powerful magnets to show pleural effusions and tumors. Arterial blood gas In arterial blood-gas sampling, a small amount of blood is taken from an artery, usually in the wrist. The blood is then checked for oxygen and carbon-dioxide levels. This test shows how well the lungs are taking in oxygen. Thoracentesis Once the presence of an excess fluid in the pleural cavity, or pleural effusion, is suspected and location of fluid is confirmed, a sample of fluid can be removed for testing. The procedure to remove fluid in the chest is called a diagnostic thoracentesis. The doctor inserts a small needle or a thin, hollow, plastic tube in the chest wall and withdraws fluid.

Parapneumonic Pleural Effusions and Empyema Thoracis -- Introduction

Uncomplicated parapneumonic effusions, which are exudative,  neutrophilic effusion. Gram stain and culture are negative, glucose level greater than 60 mg/dl, pH above 7.20. Complicated parapneumonic effusions, resulting from a bacterial introduction into the pleura. In this type of parapneumonic effusion, there is a decreased glucose level, pleural fluid is below 7.20. Cultures of fluid from complicated parapneumonic effusions are negative and rapid bacterial clearance from the pleural space, or low bacterial count may explain this. The fluid termed as complicated because it necessitates drainage for resolution. Empyema thoracis in which there is frank pus in the pleural space, or there is evidence of bacterial infection of the pleural fluid by Gram stain or a positive culture. [2] [3]

[Purulent pleurisy and empyema. With the exception of pleural tuberculosis].

Purulent collections in the pleural cavity usually occur as complications of pneumonia in immunodeficient or socially underprivileged patients. The key to diagnosis, pleural aspiration is indicated in case of sufficiently abundant collections, especially in patients with fever. Exploratory puncture is a therapeutic emergency, allowing optimal antibiotic therapy when a causal germ is isolated and drainage of the purulent collection. If there is the slightest doubt, imaging techniques should be used to guide the puncture. Drainage is essential and is indicated whenever the aspiration fluid is purulent, contains, germs or the chemistry suggests major bacterial colonisation (acid pH, low glucose, high lactic acid dehydrogenase). Local injections of fibrinolytic agents improve drainage. Complete recovery without sequellae is usually achieved. Physical therapy, provided early and for a prolonged period, helps improve the prognosis. Early care reduces the risk of recurrence of this potentially severe condition.