# Critical Care Medicine: Approach to Clinical Complications in Emergency Care and Practice

Sidharta Chatterjee

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# Critical Care Medicine: Approach to Clinical Complications in Emergency Care and Practice

SIDHARTA CHATTERJEE<fnref n="1" />

Principles and practice of emergency medicine and critical care are not just grounded on the basic tenets of “care”— but more profoundly, on the meticulous understanding and management of every matters of clinical urgency. Critical care undertakes the care of an ailing patient who presents with life-threatening illnesses often compounded with serious (multi)organ dysfunctions. Beyond a human touch which is a prerequisite— it also mandates diagnostic reasoning and clinical judgment skills to render any benefit to the critically-ill and indisposed patient. This often requires bringing forth the combined clinical decision-making abilities of several specialists which constitute a broad domain of clinical and emergency care. Essence of good critical care stems from several established protocols: e.g., early diagnosis, anticipation of possible complications, and foremost— dynamic stabilization of the critically ill (hemodynamic stabilization, metabolic optimization, etc.). This paper in the foreground, intently looks at the approaches of the intensivists to a critical illness, and attempts to delineate about how they apply wisdom, skills, and ‘intuitions’ to cure— as well as to gain a better perception of the matters of urgency in critical care medicine. While in the background, it reviews the rationale for understanding the management of complex clinical conditions characterized by shock— which still remains an important cause of complications leading to organ failure and dysfunction that contributes to high degree of mortality in the ICU. Furthermore, this paper analyses the central protocol, prognostic factors and therapeutic interventions that are being followed to manage complications of shock or related severe syndromes (Disseminated intravascular coagulopathy). Finally, the paper discusses about what kind of marginal approaches exists or might be undertaken to break the gridlock of decision “freeze” if it occurs when the last few attempts to salvage a critically compromised patient with multi-organ dysfunction fails to save a life.

*Keywords:* Critical care, DIC, emergency medicine, multi-organ dysfunction, shock

## I. INTRODUCTION

Virtually all severe cases of burn, trauma, acute myocardial infarction (AMI) or infection (sepsis, pneumonia, malaria) are accompanied by varying degrees of shock. Acute respiratory distress syndrome, sepsis, septic shock, bleeding and multiple system organ failure constitute the major causes of mortality in most ICUs [28]. In most cases of emergencies encountered in the critical care unit, shock is one of the most common and presenting symptom accompanying the primary critical illness (i.e. trauma, sepsis) of a critically ill patient admitted to an ICU [30] which requires urgent medical interventions. Spahn *et al* reports that about one-third of all trauma patients with bleeding present with a coagulopathy upon hospital admission [27]. Bleeding due to traumatic injuries is also one of the primary causes of shock. The physiopathology of shock is a complex phenomenon characterized by widespread tissue hypoperfusion from reduced blood flow and diminished cardiac output [8]. It may develop from any pathological condition that severely disrupts the internal homeostasis of the body; i.e., due to sepsis (gram positive toxemia and gram negative bacterial endotoxemia), haemorrhage, myocardial infarction, trauma, or burns [1]. The sequel of events that follows the pathogenesis of shock [16] contributes to high degree of mortality and morbidity from complications arising out of organ failure or multiple organ dysfunction [3]. In fact, multi-organ dysfunction syndrome (MODS) [6] which arise from many

<footnote n="1">¹ Independent Clinical Investigator
Email: sidharta123@yahoo.com</footnote>
pathophysiological or diseased states (e.g., burns, trauma, haemorrhage, pancreatitis or other acute and persistent inflammatory states), is the leading cause of death in the ICU [6], [24]. In particular, septic shock carries a high mortality rate and predisposes to organ dysfunction and severe bacteraemia due to complicating pathophysiology which worsens the clinical scenario. Early identification of sepsis and accurate diagnosis of underlying infections using expert clinical tools (screening electronic alert tool for severe sepsis) [9] or biomarkers [10] reduce mortality [17] from shock. Worldwide, septic shock is a critical complication from bacterial sepsis that is responsible for 18 million ICU admissions per year [1]. It is also one of the most frequent acute medical emergencies encountered in the emergency department. However, shock is not just the only presenting pathophysiological syndrome that critical care specialists deal with, but in fact any other persistent inflammatory states or chronic illnesses like liver cirrhosis, Cancer, or AIDS complicated by Multidrug Resistant Tuberculosis (MRT) in their terminal stages require critical monitoring and care. Complications arising out of surgical emergencies or status syndrome (status epilepsy) that also require admission to the ICU necessitate close monitoring of the patient. Several scoring systems that include Acute Physiology and Chronic Health Evaluation (APACHE II), the Simplified Acute Physiology Score (SAPS II), and the Multiple Organ Dysfunction Score (MODS) are in place to assess care, monitor resuscitation and progress, measure outcomes, and evaluate morbidity and mortality in the emergency department (ED) [25].

## II. Guidelines and Protocols for Management of Critical illnesses

*Clinical judgement and decision making in the ER*

Guidelines and protocols in the form of knowledge base about how to approach and manage the critically ill have been outlined by several consultative bodies as well as by organizations having expertise in formulating protocols for treatment guidelines [25]. The American College of Critical Care Medicine (ACCM)—the consultative body of the Society for Critical Care Medicine (SCCM) outlines several administrative protocols and clinical practice parameters which are being continually developed and updated for providing better patient care and promote “best practices” to improve patient outcomes [26]. Similarly, The International AIDS Society (IAS-USA) also publishes clinical guidelines for practicing physicians who are responsible for treatment of AIDS and terminal complications arising out of AIDS. Indeed, great transformations have taken place in the domain of critical care and emergency medicine within the last few decades. With the rapid advancement of scientific technology, diffusion of scientific knowledge in the form of evidence-based principles into medical practice has increased the quality and efficacy of therapeutic implementations [28]. Clinical judgements are now based on scientifically accumulated evidences which form the core philosophy of the practice of evidence-based medicine. The influence of technology on reducing morbidity and improving mortality in critically ill patients owes much to the routine use of advanced life-support systems, and by following well established clinical guidelines and protocols [7]. Advancements in ambulatory care and intensive stabilization of a critically ill patient during mobilization to a hospital have largely improved the survival rate among those patients. Such transformations have not only generated new knowledge, but have brought medical care within the close reach of the many critically ill who would have been left out for the acute lack of access to primary and secondary healthcare— more so in the developing countries. With enormous growth in the number of critical care units (ICU/ITU), and parallel advancement in medical care characterized by growth in clinicians specially trained, experienced, and having competence to treat and manage complex clinical problems, this domain contributes greatly to the profession of medicine [1][7][30]. It must be born in mind that a critically ill patient needs constant care and observation: e.g., monitoring of his or her vital parameters, hemodynamic status supportive of reflexive actions to acutely emergent complications— those
complicated by sepsis or single or multiple organ failure, and finally, complications arising out of polytrauma. Working guidelines to manage life-threatening illnesses in the ICU is complemented by linking knowledge with expertise and experiences of specialists who work as a team where technology acts as an adjunct to a doctor's skill and expertise. For instance, critical illnesses complicated by polytrauma and severe infections (i.e., burn, subarachnoid haemorrhage, or severe endotoxaemia following) carry a high morbidity and mortality rate in the ICU, and the prognosis is often poor in acute organ system failure as occurs in acute renal failure due to shock⁷. Some potentially life-threatening illnesses turn out to be irreversible, in spite of the best attempts of the attending intensivists. There is growing evidence supporting the fact that patients with 3 or more organ system failure for more than 3-4 days have a high mortality rate of about 98% [7].

Once again, it shall be born in mind that critical illness is most often characterized by primary presenting symptoms accompanied by pain and anxiety. Therefore, control of pain and alleviation of anxiety using analgesics and anxiolytics should be supplemented with adequate hemodynamic stabilization, and fluid and electrolyte replenishments to maintain adequate tissue perfusion and cellular metabolism. The primary goal of emergency care is to stabilize the patient with appropriate measures, treat the immediate presenting symptoms, and *do no harm* since inappropriate action costs lives (*Primum Non Nocere*). Recognition of the presenting problem and accurate diagnosis backed up by essential support systems are essential to manage life-threatening medical emergencies. In cardiorespiratory depression, support systems—including ECG monitoring, positive pressure ventilation, arterial blood gas, and other monitoring gadgetry for close observation of cardiopulmonary and renal hemodynamic status to evaluate a patient’s individual physiological adaptations to disease and its treatment should be closely monitored. A motivated and dedicated team of specialists could provide better patient care supplemented by sound clinical judgment and acumen for judicious use of invasive gadgetry to manage medical or surgical emergencies. Particularly relevant in the developing countries, where resources are scarce, judicious allocation of medical resources and its optimal use for approaching a critically ill patient relies mostly on clinical acumen and expertise. However, in spite of every effort and exertion, therapeutic decision-making and interventions often “freeze” under complex clinical settings wherein, despite all interventions and manoeuvres, it becomes extremely difficult to stabilize a critically indisposed patient, and the inevitable death can only be prolonged with vigorous life-support. In effect, the decision-making do not actually *freeze*, but rather, there remain very few options open for any further therapeutic interventions to salvage the patient’s life. Here, it shall be recalled that two aspects counterpale the conundrum: rationality on the part of the physician, and emotion on the part the patient’s relatives. This however, do not question the limits of clinical rationality, but rather calls for further learning and action from “hard experience”[2] gained from such failed attempt. This paper endeavours to address these critical aspects of clinical decision-making to delineate what kind of marginal approaches exists or might be undertaken to break such a gridlock of decision freeze by contemplating on how emergency physicians and intensivists apply wisdom, skills, and ‘intuitions’— not just to cure—but also for a better perception of the matters of urgency in such critical conditions.

### III. Acute Medical Emergencies: Knowledge Meets Practice

Implementing therapeutic procedures on critically ill patients require knowledge and understanding of the pathophysiology of the underlying medical conditions [25] [26] [28], which is often superseded by enormous complexity of the complications arising out of the primary presenting symptoms. Emergency units and critical care centres are specially equipped to deal
with life-threatening medical complications where the solitary objective is to stabilize the patient by all means and methods prescribed in medical practice. Some of the most common causes of morbidity and mortality in the ICU patients are due the complications arising out of severe sepsis and shock. The table lists acute medical emergencies which are among the common reasons for admissions to an ICU [37];

<figure><img src="image_2.png" /><figcaption>Table 1. Classification of Medical Emergencies (adapted from Acute Medical Emergencies: The Practical Approach, 2001, BMJ)</figcaption></figure>

Despite the best efforts of the attending emergency teams, some common mistakes and errors in judgment often results in avoidable serious adverse clinical episodes which leads to death of the patient. However, and in most other cases, it is not often on account of misdiagnosis or clinical error, but due to overt complications from common medical conditions which is the cause of high mortality rate among patients who would have had a better chance of survival if those complications could have been contained.

## IV. Pathogenesis, Pathophysiology and Management of Shock

One of the primary factors that specialists generally deal with in the emergency unit is the management of shock [30]: Shock may be simply defined as an "acute circulatory collapse which leads to severe tissue hypoperfusion and cellular injury". A more workable definition of shock is provided by Simeone [35] who states that (shock may be defined as): "a clinical condition characterized by signs and symptoms which arise when the cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to provide organs and tissues with adequate blood flow." [35] Most patients referred to the critical care unit /ICU comes with an acute ailment; e.g., severe trauma, poisoning, crush injury, burns, haemorrhage and bleeding, fall or fracture (bone trauma), ballistics injury, motor vehicle accidents, or due to acute complications from fulminant infections. Some of the most life-threatening conditions which fall in this critical category are due to organic diseases which include myocardial infarction (MI), cerebrovascular accident (CVA), cardiorespiratory arrest (due to cardiac arrhythmias), acute respiratory distress syndrome (ARDS), or stroke. Almost all of these conditions present with some form of hemodynamic disturbances, shock and/or organ dysfunction. While acute ischaemic diseases (IHD) of the heart presents as cardiogenic shock, severe hypotension due to massive haemorrhage is classified as hematogenic or hypovolemic shock. According to a classification by Blalock [34], shock may be categorized into:

i. Hematogenic (oligemic)

ii. Neurogenic

iii. Vasogenic, and

iv. Cardiogenic
A simple way to classify shock is to consider three categories— hypovolemic, cardiogenic, and septic or distributive shock. Although the initial pathogenesis may be different for these four different kinds of shock, yet they are interrelated dysfunctions which ultimately results in hypovolemia, low cardiac output, tissue hypoxia, and compensatory mechanisms characterized by reflex sympathetic stimulation which functions as an endogenous life-saving mechanism. The varying clinical pictures may be different for different types of shock, but the ultimate pathophysiological sequel is almost similar in all four types of shock; i.e., hypoxemia, fall in cardiac output, and hypoperfusion. The excess of adrenosympathetic activity is also common to most types of shock. However, this compensatory mechanism which restricts blood flow to other less dependent organs in times of crisis in order to maintain circulation to the brain and the heart— although very limiting, it results in severe hypo-perfusion of the kidney at the expense of the brain. Shock is well characterized by cellular hypoxia which leads to inadequate delivery of oxygen and nutrients to the tissues, and reduced clearance of metabolites from the cells [8], [30]. Although shock is *not* by itself an inflammatory reaction but an acute hemodynamic disorder (although Type I hypersensitivity reactions can induce potentially dangerous anaphylactic shock due to release of the inflammatory mediators and anaphylotoxins, e.g., C3a and C5a), nevertheless, it may result from acute inflammatory conditions as such; e.g., acute pulmonary embolism, acute pancreatitis or acute myocardial infarction. Shock may elicit release of mediators and cytokines from injured endothelial tissues which further potentiates the action of cellular injury at the molecular level in the progressive-irreversible phases of shock.

The clinical course of shock is arbitrarily divided into three phases or stages: (i) Stage I is non-progressive, (ii) Stage II is progressive, and (iii) Stage III which is irreversible [8]. It is the last stage (Stage III) which is in most case irremediable despite correction of hemodynamic instabilities, and hence it is fatal. The reason for this is due to the fact that although compensatory mechanisms are triggered in the first stage of shock, if left untreated, tissue hypoperfusion sets in the progressive stage of shock. With persistent oxygen deficit and accumulating metabolites the pH level begins to fall inducing acidosis. With a fall in pH, and a rise in accumulating metabolic products of anaerobic glycolysis which is lactic acid, *metabolic acidosis* sets in which induces widespread tissue hypoxia. It is in this stage when vital organ dysfunction begins to set in due to pooling of blood in the microcirculation causing a further reduction in cardiac output. Severe hypoperfusion of the kidney results as a consequence which leads to acute tubular necrosis with resultant anuria and renal failure [4], [6]. While Helmut *et al* [12] have studied the outcome of daily dialysis in patients with acute renal failure, Conlon reported that patients who developed acute renal failure following Coronary artery bypass graft surgery (CABG) requiring hemodialysis carries a poor prognosis [33]. Nevertheless, the second stage of shock is rapidly progressive, but may still be reversible provided that prompt treatment is initiated, and, the initiating pathogenicity is controlled. At the same time, it requires vigorous correction of hemodynamic alterations and reversal of metabolic acidosis. Vasopressors and corticosteroids are used, besides fluid and blood transfusions which usually correct most of the vascular phenomena at this stage if the shock is not compromised by sepsis (endotoxemia). Initially, in the reversible stage, several compensatory mechanisms are triggered which helps to maintain organ function and perfusion. These include— baroreceptor and chemoreceptor reflexes, release of catecholamines from the adrenal medulla, aldosterone from the adrenal cortex, and stimulation of the renin-angiotensin system which helps to retain fluid by increased tubular reabsorption of water and electrolytes. Any deficiency in these compensatory mechanisms involving renin-angiotensin system in the kidney at this stage is almost always fatal. It shall be noted that Angiotensin II is a potent vasoconstrictor agent released from the kidney, and it was often supplemented in the treatment of shock when other catecholamines fail to
ameliorate the worsening condition. In response to hemorrhagic shock, erythropoietin is released from the kidneys which stimulate formation of new red blood cells to maintain the normal haematocrit (PCV) level. Nevertheless, all these reflex actions are mediated to maintain cardiac output and tissue oxygenation. Administration of sympathomimetic vasopressor agents and release of endogenous catecholamines increases both inotropic [32] and chronotropic actions of the heart, resulting in tachycardia and peripheral vasoconstriction. Vasoconstriction as a compensatory mechanism tends to reduce bleeding in severe haemorrhage and helps maintain blood pressure. To be noted, all these mechanisms are triggered in response to initial hypovolemia and vasodilation. A potential complication which can arise in the progressive stage of shock is disseminated intravascular coagulation (DIC or consumption coagulopathy) which may further complicate the clinical settings. Ironically, this complication is a paradox and poses as a great challenge to the attending intensivists and physicians, and which is discussed in some detail in the subsequent section.

There is substantial evidence involving cellular hypoxia causing release of chemical mediators from the endothelial walls of blood vessels, some of which are potent mediators implicated in the induction of shock. Also, endotoxin-mediated activation of cellular phagocyte system release IL-1 and TNF-α which comprises of the key elements of septic shock [8]. Furthermore, release of secondary mediators that include prostaglandins and platelet activating factor (PAF) potentiates inflammatory effects while nitric oxide (NO) induce vasodilation. This is a hallmark in shock since acute hypovolemia from massive haemorrhage causes vasodilation due to actions of potent mediators and cytokines released on account of endothelial tissue injury. Acute blood loss reduces blood flow through the splanchnic organs and the compensatory mechanism attempts to shunt the blood away to the most vital organs— brain and the heart. To be noted, severe hypovolemia causes a drastic drop in systolic blood pressure characterized by intense vasodilation and the ensuing hypotension reduces stroke volume and cardiac output. The reactive vasoconstriction due to reflex stimulation of the sympathetic nervous system while activation of neurohumoral mechanisms are counter-regulatory mechanism to offset potentially fatal vasodilation which causes severe hypotension-induced cellular hypoxic injury. Although cellular hypoxia is injurious to almost all the cells of the body, particularly vulnerable organs are those which are vital; e.g., brain, heart, lungs, liver and the kidney. Reduction in cardiac output stimulates reflex activation of the sympathetic nervous system as a compensatory mechanism. This resulting reflex stimulation of the sympathetic nervous system causes increased secretion of endogenous catecholamines (adrenaline & epinephrine) from the adrenal medulla which induces vasoconstriction that attempts to maintain normal stroke volume and blood pressure in order to preserve the circulation of vital organs, most importantly— the brain. However, organ dysfunction is elicited when the systolic blood pressure falls below 90 or <86 mm Hg. Brain (cerebral) auto-regulation collapses under systolic blood pressure of about <65 mm Hg (See Ganong's Medical Physiology) while hypoperfusion of the brain cells further complicates the pathogenesis of shock. Unless the underlying hypovolemia is rapidly corrected (along with control of specific causes of shock) with vigorous fluid (blood/plasma/i.v. fluids etc.) transfusions (to maintain the cardiac output), and medications (vasopressors, corticosteroids), the patient dies. A complete discussion of diagnosis, monitoring and the medical management of shock is beyond the scope of this paper; readers may refer to Mtaweh et al [30] for a more comprehensive analysis of the management of shock. However, some general approaches to management of shock may be underlined which follows—

i) Management of specific and underlying causes— i.e., myocardial ischemia (MI) and myocardial infarction [11], severe sepsis, bleeding, and
ii) Monitoring of clinical laboratory parameters, non-invasive cardiac output monitoring, renal output, biomarkers, and arterial pulse wave analysis.

iii) Control of related hemodynamic alterations— e.g., correction of hypovolemia due to bleeding and haemorrhage with blood transfusions to restore lost blood, and fluid and electrolyte replenishments to restore normal fluid and electrolyte homeostasis.

The general protocol and a simple guideline for ICU checklist and management of shock are depicted in Fig.1.

<figure><img src="image_3.png" /><figcaption>Fig. 1 General Protocol and Guideline indicating Checklists for Management of Shock: Adapted from SCCM & from Trauma Care: Echelon Concept and its Relevance: SK Kochar, *Principles and Practice of Trauma Care*.</figcaption></figure>

As much as the brain and the heart are susceptible to severe hypotension, kidneys are particularly prone to damage under severe hypotensive crisis, as in shock; i.e., due to prolonged tissue hypoperfusion—which however, results in acute renal tubular ischemic injury, culminating into renal failure. Administration of dopamine at low dose helps to maintain renal perfusion in shock which increases renal blood flow and the glomerular filtration rate (GFR). Dopamine improves renal hemodynamics when used in low doses in shock. The use of low dose dopamine (LDD) to treat or prevent renal dysfunction in shock [13] has been widely acknowledged and has become a routine clinical practice for “renal dose” dopamine [15]. However, Lauschke et al [22] states that there is no established therapeutic efficacy of using LDD in patients with acute renal failure; rather, such a practice can worsen renal perfusion in patients with ARF. Nevertheless, previous studies by Carcoanna and Hines [15], and later by Karthik and Lisbon [38] have stated that Low-dose dopamine (LDD) has been shown to increase renal blood flow in animal and in human volunteers. While Jones and Bellomo [23] points to the fact that there is insufficient evidence in support of the use of low dose dopamine use in ARF, Lherm [14] examined renal effect of both low dose dopamine (LDD) and catecholamines on patients with septic shock, with no new surprise. However, it shall be recalled that dopamine has dose dependent effects on dopamine receptors as well as on α and β adrenergic receptors. This is in fact one of the reasons for application of dopamine in shock syndrome. An ideal approach most commonly practiced by
emergency specialists to manage shock is to use drugs that help induce peripheral vasoconstriction without affecting vital organ perfusion while at the same time maintaining cardiac output (by measuring cardiac index) and stroke volume. It shall be recounted that complications of shock resulting in ARF carries a high degree of risk associated with high mortality and morbidity rate in the ICU [3], owing to resultant uraemia which is toxic to the brain [23]. Hence, hemodynamic stabilization should be promptly instituted to avoid any further complications.

# V. Managing Complications of Shock: Multi-organ Dysfunction due to DIC

Shock may predispose to multiple organ dysfunction and failure. One condition that merits discussion among others is acute renal failure (ARF) [4] which is believed to be the common setting of critical illness— or presents itself as a presenting complication from shock due to polytrauma, disseminated intravascular coagulopathy (DIC) and sepsis, or due to any of the above mentioned critical conditions in Table 1. Another complicating scenario may arise in patients with shock from myocardial infarction, since such patients are prone to the development of DIC (also known as consumption coagulopathy) [4]. It becomes an intensivist's nightmare to manage a patient in shock eliciting symptoms of DIC already compromised by acute renal failure. Therapeutic decision-making under such an emergent complexity makes patient management more complex [30]. As Delaney et al [30] points out, management of critically ill patients is complex, involving multiple interventions and processes. It is here where therapeutic decision may “freeze” which can complicate the already complex scenario. Freezing here means lack of options or opinions about how to salvage the life of the patient when it is apparent that little progress can be made even with the best possible therapeutic interventions. We shall conclude with a discussion on the management of DIC in septic shock and the reasons behind poor prognosis associated with it even under best clinical settings.

DIC is an acute thrombohemorrhagic disorder which may occur from obstetric complications (retained dead foetus), bacterial sepsis (septic shock), massive trauma, crush injuries, snake bite (viper), or other vascular disorders and injuries [5], [7]. Severe whole body trauma of extreme nature, or isolated brain injury can cause DIC as well [20]. Shock induced hyperfibrinolysis can give rise to DIC which can contribute to severe oozing-type bleeding which is later followed by extensive microvascular thrombosis [20]. Microvascular thrombosis is one of the causes of organ dysfunction and may lead to organ failure. DIC is characterized by clinical symptoms of bleeding and formation of microthrombi, or both, at the same time. Formation of thrombi within the microcirculation blocks the minute arterioles that cause tissue hypoxia, while consumption of coagulation factors results in delayed blood clotting or increased fibrinolysis due to elevated levels of plasmin which leads to bleeding tendencies (hemorrhagic diathesis) [5]. It is a disorder of the coagulation cascade due to abnormal activation of the coagulation and clotting factors which cause intravascular thrombosis within the microcirculation. When the coagulation factors are consumed, lack of clotting factors induces increased fibrinolysis which leads to bleeding within the microvasculature, organs, skin, and in the brain; hence also called consumption coagulopathy [18], [19]. It is one of the potent causes of multi-organ dysfunction. The diagnosis of DIC is rather problematic. Although laboratory tests indicate prolonged ↑prothrombin time (PT), ↑partial thromboplastin time (PTT), thrombocytopenia, and increased fibrin degradation products, none of these are specific to conclude a DIC pathology [5]. However, signs of bleeding in the ICU raise the first alarm when such bleeding cannot be easily controlled (due to ↑ PT and ↑ PTT). Formation of microthrombi in patients already compromised by renal ischemia due to shock poses as a challenge to the attending physicians. Treatment protocol refers to control of
the underlying disorder, i.e., sepsis or shock, along with transfusion of FFP, cryoprecipitate, platelet concentrates (to manage thrombocytopenia) and thromboprophylactic strategies for all patients following traumatic injury [27]. Injudicious use of heparin may induce bleeding and haemorrhage while antifibrinolytic agents may prove dangerous because of increased risk of widespread intravascular thrombosis (microthrombi formation). A reciprocity (or trade-off) must be attained to ameliorate the symptoms and control DIC. Yet, control of bleeding must be achieved to avoid any further hematogenic shock. This not only poses as a therapeutic paradox— but presents as a physician's nightmare. Indeed fibrinolytics may help to dissolve microthrombi, but it may prove to be dangerous because of risk of bleeding. Thrombosis and bleeding in trauma patients is a complex phenomenon which is a hallmark of DIC [20]. While at the same time antifibrinolytics may prove to be fatal because of the above mentioned reason. It shall be acknowledged however, that shock can either be the result of DIC or may itself cause DIC (due to shock from severe whole body trauma).

Most complex clinical phenomena like DIC are effectively managed through team effort. When options run out, to save a life, ED physicians fight rationality with emotion, and meticulous judgment and decision-making based on evidence-based medicine does more good than harm. Fundamental basis of critical care for terminally ill and severely traumatic patients is to stabilize the patient first, and salvage his life by all means within rational limits of medical practice. The concept of disease is based on scientific evidence, and hence, therapeutic interventions should also be based solely on scientific principles. Clinical judgments in critical cases may go wrong, but judicious use of technology, information and gadgetry may elicit new hidden clues in complex clinical settings which call for further learning and action from “hard experiences” of success and failure. This would minimize decision “freeze” under complex clinical settings.
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