Complications table

renal dysfunction

short termhigh

Transient oliguria is common and is related to hypotension. Rarely, anuria occurs.[273] Acute kidney injury is relatively common but is rarely associated with histological change or with any need for long-term renal replacement therapy.

Correction of volume depletion and hypotension generally reverses oliguria.[273]


short termhigh

Volume depletion is caused by reduced oral intake, increased venous capacitance, increased fluid losses due to pyrexia, capillary leakage leading to oedema, tachypnoea, diarrhoea, and possibly bleeding. Persistent hypotension is often due to a combination of low systemic vascular resistance, hypovolaemia and reductions in cardiac output from myocardial failure, excessive positive end-expiratory pressure, or acidosis.

Fluid resuscitation is given with either colloids or crystalloids, and early central venous pressure monitoring is indicated if rapid response is not achieved. Vasopressors can be started for persistent hypotension or inotropes for myocardial failure. Caution is required to prevent tachyarrhythmia.

acute respiratory distress syndrome (ARDS)

short termmedium

Respiratory failure often progresses quickly and is indicated by a respiratory rate >30/minute, even though arterial oxygen levels may be normal.

ARDS may resolve completely or can progress to fibrosing alveolitis with persistent hypoxaemia.[272]

Intubation and ventilation reduce respiratory muscle oxygen demand and the risk of aspiration and cerebral anoxia.[273] Lung protective ventilation (low tidal volumes) should be used.[266] Tidal volumes should be reduced over 1 to 2 hours to a target of 6 mL/kg of predicted body weight. Minimum positive end-expiratory pressure is recommended to prevent lung collapse at end expiration.[43]

myocardial dysfunction and failure

short termmedium

Myocardial dysfunction with biventricular dilatation is a recognised complication of sepsis, but is usually transient and not commonly severe. Death from myocardial failure is rare.[177] Circulating myocardial depressant factors are thought responsible.

After adequate filling pressures have been achieved, inotropic agents should be considered to maintain an adequate cardiac index, mean arterial pressure, mixed venous oxygen saturation, and urine output.

Clinicians should define specific goals and desired end points of inotropic therapy in patients with sepsis and titrate therapy to those end points. These end points should be refined at frequent intervals as patient's clinical status changes.[177]

multiple organ system failure

short termmedium

The inflammatory response in sepsis causes widespread tissue injury. Multi-organ dysfunction may be partly caused by apoptosis of immune, epithelial, and endothelial cells and a shift to an anti-inflammatory phenotype, compounded by impaired organ perfusion due to hypotension, low cardiac output states, circulatory microthrombi, a disordered microcirculation, and tissue oedema.[266]

Failure of each additional organ increases the average risk of death by 15% to 20%. Lung dysfunction tends to occur early and persists. Serious central nervous system dysfunction or liver function often occur hours to days after sepsis onset and persists for variable periods of time. Most organ failures resolve within a month in surviving patients.[273]

Treatment of multi-organ failure in sepsis is primarily supportive. It includes effective antibiotic therapy, goal-directed therapy (to reverse hypotension, anaemia, coagulopathy, bleeding, and shock), and standard supportive intensive care setting care. This may include dialysis, ventilatory support, and sedation.

hepatic encephalopathy

short termlow

Liver dysfunction may lead to hepatic encephalopathy, especially in those with established chronic liver disease.[269] Hepatic encephalopathy is thought to result primarily from ammonia entering the brain due to absorption from the gut bypassing effective hepatic clearance. This causes intracellular cerebral oedema and electrolyte abnormalities.[270]

The mainstay of therapy includes laxatives to empty the bowel, prevention of GI bleeding, and avoidance of sedative drugs, which further suppress consciousness. A low-protein diet is not recommended as these patients are often malnourished with muscle wasting, which is an important negative prognostic indicator for hepatic encephalopathy and cirrhosis. These patients’ protein requirements are also relatively higher than those of healthy patients. Protein intake should be 1.2-1.5g/kg/day.[271]

disseminated intravascular coagulation (DIC)

short termlow

Occurs in sepsis when leukocytes and endothelial cells are activated or injured by toxic substances released during infection or shock. The injured cells generate tissue factor on the cell surface, activating the coagulation cascade. In acute DIC, an explosive generation of thrombin depletes clotting factors and platelets. This activates the fibrinolytic system.

DIC leads to bleeding into the subcutaneous tissues, skin, and mucous membranes occurs, along with occlusion of blood vessels caused by fibrin in the microcirculation.

Treatment of the underlying disease is the mainstay of management of either acute or chronic DIC, with blood products to control bleeding.[274]

neurological sequelae

long termmedium

The incidence and severity of complications from sepsis depend on the pathogen, duration of disease, age, and presence of comorbidities.

Focal neurological deficits and hearing loss occur in up to 30% of patients with bacterial meningitis. The mortality and morbidity is higher for pneumococcal meningitis than for meningococcal meningitis.

Polyneuropathy occurs in 70% of patients with sepsis and multi-organ failure. The use of neuromuscular blocking agents may increase the severity of polyneuropathy.[275][276]

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