Care of the critically ill patient

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Introduction to critical illness

Intensive care for complex and potentially life threatening illness is required by about 2.5% of patients admitted to major Australian hospitals. Intensive care units (ICUs) have been widely available for approximately 30 years, but now there are about 200 ICUs in Australia, of which about 60% are level 3 or the most sophisticated. Intensive care has permitted the survival from many types of hitherto fatal illness or injury, with the interesting consequence that pathophysiological responses are now seen which could never have originally been adaptive and which may in turn lead to new therapeutic opportunities.

Intensive care is inevitably expensive, but about 85% of patients survive, most with good quality, long-term outcomes (Pathways of critical illness.). Coexistent medical conditions substantially influence patient outcome. Prognosis is worsened when there is coexistent ischaemic heart disease, diabetes, peripheral vascular disease, severe chronic obstructive airways disease or malignancy. In the absence of these co-morbidities, advanced age is not a major independent factor in short-term prognosis. Reliable prediction of patient outcome would greatly assist patient selection, clinical management and resource allocation, but models of mortality prediction based statistically on scoring systems for critical illness are suitable so far only for group comparisons and not for individual patient assessment.

Pathways of critical illness.

Causes of critical illness

The chief categories of causes of critical illness and thus admission to ICU are shown in the figure.

Severe infection remains the most common and concerning problem in the care of seriously ill patients in hospital. It provides the most important link between either underlying or complicating illness and serious conditions such as circulatory failure, respiratory failure and organ failure. The definitions of infection and related phenomena such as sepsis and septic shock are shown in Pathways of critical illness.. Clinically suspected sepsis occurs in approximately 10% of ICU admissions and has a mortality of 5% to 20%. Severe sepsis and septic shock has a mortality of 35% to 65% despite antimicrobial therapy and intensive life support. Survivors of severe sepsis commonly require prolonged hospitalisation due to post-sepsis multiple organ dysfunction.

The incidence of sepsis is thought to be so high because of continually emerging antibiotic resistance of micro-organisms and because of the complex and invasive procedures on increasingly sick patients that characterise modern hospital practice. The most commonly isolated organisms are Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus pyogenes, various enterococci, Gram-negative bacilli and Candida spp. When sepsis is suspected but the site remains unknown despite an appropriately thorough clinical investigation, the abdomen and lungs are the two most likely sites, together with intravascular catheters if such are in place.

The bodily responses to sepsis are indistinguishable from those due to non-infective inflammation or indeed to severe injury itself. The systemic response to injury in general is referred to as the systemic inflammatory response syndrome (SIRS) (Table 15, “Definitions in sepsis*”). The definition of SIRS describes a widespread inflammatory response to a variety of clinical insults, not all of which necessarily involve bacterial infection. The constellation of clinical, haematological, and biochemical signs typically found in the presence of infection can often be observed in the absence of any identifiable infection, as with pancreatitis, trauma, burns, rhabdomyolysis, necrotic tissue and cardiopulmonary bypass.

Over the last 10 years, detailed study of the timing and associations of elevated levels of cytokines, eicosanoids, oxygen radicals, proteases and autacoids in the plasma of patients with septic shock has advanced our understanding of this complex and potentially lethal clinical state, which may represent an imbalance among the various host responses to tissue injury. Experimental investigations have shown that interruption of the complex inflammatory mediator cascade can lead to striking benefits in a wide variety of animal models of infection or uncontrolled inflammation. However, until recently it has been a recurrent finding from Phase III human studies that these apparent benefits are either not confirmed or are sufficiently modest in magnitude that clinical application of the therapeutic strategy is not worthwhile. The first agent to convincingly overcome this therapeutic barrier may be the biopharmaceutical agent drotrecogin alfa (activated) [recombinant human activated protein C]. This very expensive therapy has been associated with a 20% relative reduction in mortality from severe sepsis.


The key to resuscitation is that it must be prompt and complete, with restoration and maintenance of an adequate circulating blood volume (i.e., treatment of hypovolaemia). This is a fundamental requirement in all seriously ill patients. Without adequate blood volume expansion, inotropes and other therapies are less likely to be effective, and organ function is compromised. The choice of fluids for acute resuscitation is less important and remains controversial, with no universal recommendation able to be made except that replacement of losses should usually reflect the major deficit caused by the underlying disease process. Both crystalloids (e.g. 0.9% sodium chloride, compound sodium lactate or Hartmann's solution) and colloids (e.g. 4% albumin, polygeline) are available, as well as hypertonic saline (3%) and blood products. Saline 0.9% or albumin 4% in saline 0.9% have been demonstrated to result in equivalent patient outcomes from critical illness, although the overall ratio of the volume of albumin to the volume of saline administered was approximately 1 : 1.4.

Fluid resuscitation may need to be substantial because, in addition to obvious losses and to anticipated third-space needs, there is often extra volume required due to vasodilatation, capillary leak and blood flow maldistribution. Fluid resuscitation is complete if blood flow is restored (i.e. the haemodynamic goal) or if cardiac filling pressures are maximised, whichever is first. If a satisfactory haemodynamic goal has not been achieved despite maximised cardiac filling pressures and thus repair of hypovolaemia, inotrope therapy is required if myocardial contractility is impaired and/or vasopressor therapy is required if blood pressure is inadequate (e.g. in the low systemic vascular resistance syndrome). In complex situations, sophisticated haemodynamic monitoring is used to ensure that normovolaemia is achieved and maintained and to guide added pharmacological therapy.

Table 15. Definitions in sepsis*
* Septicaemia is no longer a recommended term as it was thought to be ambiguous (for practical purposes it was a synonym of sepsis).

A microbial phenomenon characterised by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms.


The presence of viable bacteria in the blood.

Similarly, for other classes of microorganisms including fungi, viruses, parasites and protozoa.


Systemic Inflammatory Response Syndrome

Consisting of two or more of the following: temperature >38°C or <36°C, heart rate >90 beats/min, respiratory rate >20 breaths/min or Paco2 <32 mm Hg, leukocyte count >12 000 cells/mm3 to >4000 cells/mm3, or >10% immature (band) forms.


SIRS as a result infection.

Infection is often clinically diagnosed and the absence of positive cultures does not exclude the diagnosis.

Severe sepsis

Sepsis associated with organ dysfunction, such as coagulation abnormalities, altered mental status, or oliguria


Hypotension, defined as a systolic blood pressure <90 mm Hg or a reduction of >40 mm Hg from baseline in the absence of other causes for hypotension (such as anaesthesia or antihypertensive medication).

Studies may require this condition to be present for a definite period, often >1 h.

Septic shock

Sepsis with shock, despite adequate fluid resuscitation, along with the presence of organ dysfunction and perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status.

An adequate fluid challenge was not defined, but many studies have specified an intravenous infusion of isotonic fluid, colloid, or blood products to restore the effective circulating blood volume. Other studies nominate a volume of 500 mL to satisfy this criterion. Patients who are receiving inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured.

Organ dysfunction and failure

Current functional assessment of organ damage emphasises a continuum of progressively worsening organ dysfunction rather than an arbitrary division between normality and failure. Thus, older terms such as ‘multiple organ failure’ (MOF) or ‘multiple system organ failure’ (MSOF) have been replaced by the broader term ‘multiple organ dysfunction syndrome’ (MODS). Except for the acute respiratory distress syndrome (ARDS), which is the pulmonary manifestation of MODS and which has precise (though still arbitrary) definitions set by international consensus, MODS has no universally agreed set of definitions. These definitional difficulties arise primarily because of incomplete understanding of the complex pathogenesis of MODS.

The incidence of MODS varies greatly with the patient group being considered. In uncomplicated surgery, it is rare. In serious and complicated surgical conditions, such as trauma, haemorrhage, sepsis, necrosis or shock, it is 5% to 10%. In uncontrolled sepsis, it is much higher. Available prophylaxis only halves its incidence in the patient groups at risk.

In humans, the organs most affected histologically are in descending order: the lungs, liver, kidney, heart, gut, brain, pancreas and adrenals, though it is likely that most if not all of the tissues and organs of the body are similarly affected. If the blood is considered an ‘organ’, it too undergoes profound change with the process of disseminated intravascular coagulation. If the endothelial cells are considered together, they bear much of the brunt of the systemic process, with microcirculatory dysfunction and consequent capillary leak, interstitial oedema and even haemorrhage, and later cellular infiltration.

The clinical manifestations are sequentially the systemic inflammatory response syndrome, a hyperdynamic circulatory state and hypermetabolic state, and then, after a latent period, respiratory dysfunction (within 48 h), liver and kidney dysfunction (within 1 week), persistent coma, gut dysfunction (with not only ileus and stress ulceration but also loss of barrier function and thus bacterial translocation), and nosocomial infection (initially respiratory, urinary and wound colonization and later bacteraemia and intravascular catheter infection).

The clinical picture of MODS thus progresses over about 3 weeks, by which time about half the patients will have died. Clearly, the earlier the underlying causative process is controlled, the earlier the clinical course can be aborted and the better the prognosis. Wound healing is sometimes said to give a partial guide to the progress of concomitant organ repair. The average mortality is about 50%, with most deaths occurring by 3 to 4 weeks. The mortality is higher (60%) if septic shock is present; it also increases by about 10% for each additional organ in clinical failure.

However, MODS is potentially reversible, although at the cost of complex, expensive and prolonged treatment. The average ICU stay is about a month and survivors have an average time to full rehabilitation of about 1 year.

Management of the critically ill

The detailed management of the critically ill patient is the subject of a vast literature and of many textbooks, some of them huge. But the general principles are straightforward, although their implementation can be complex and sophisticated.

  • Resuscitation and maintenance of an optimal blood volume is just as much a continuing priority as it is an initial goal in the treatment of the critically ill (as discussed previously). The maintenance of an adequate circulatory state is an ongoing task.
  • Treatment of respiratory impairment, together with circulatory management, comprise the twin pillars of life support in the ICU. Abnormalities of gas exchange and of pulmonary mechanics are common and are often severe. Specialised and sophisticated mechanical ventilation is the ultimate mainstay of respiratory support.
  • After initial resuscitation, and while circulatory and respiratory support are in train, early diagnosis and specific therapy (if any) are required. In particular, early and complete source control is essential.
  • There is much emphasis on the treatment of initial sepsis and on the prevention and treatment of complicating infections.
  • Metabolic support is essential, because malnutrition can develop rapidly and is a covariable in mortality and because adequate nutrition is required for tissue repair. Enteral nutrition is preferred if technically feasible.
  • Renal support may require renal replacement therapy (most commonly nowadays with extracorporeal continuous venovenous haemodiafiltration (CVVHDF).
  • Psychosocial support is important both for the patient and the family. The patient needs analgesia, anxiolysis, comfort and dignity, and the family needs access, information and support.
  • Intensive care requires continuous patient management by a highly skilled multidisciplinary team in a specialised environment. Meticulous attention to detail is necessary to identify problems and therapeutic opportunities as early as possible. In general, much of the care of the critically ill is founded on complex physiological support, which buys time for healing to occur.

Further reading

Dellinger RP, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for the management of severe sepsis and septic shock. Crit Care Med. March 2004; 32(3): 858–873. Erratum in: Crit Care Med 2004 Jun; 32(6):1448. Correction of dosage error in text.

Bersten AD, Soni N, Oh TE, eds. Oh's Intensive Care Manual. 5th ed. Edinburgh: Butterworth-Heinemann; 2003.

Irwin RS, Rippe JM, eds. Irwin and Rippe's Intensive Care Medicine. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2003.
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