Oxford Handbook of Critical Care (3 edn)
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Hypothermia
Clinical features
>33°C—shivering in an attempt to correct body temperature.
<33°C—neurological signs of dysarthria and slowness appear.
>31°C—hypertonicity and sluggish reflexes with cardiovascular dysfunction become life‐threatening.
<28°C—arterial pulses often impalpable. Hypothermic rigidity is difficult to distinguish from death.
Prognosis depends on the degree and duration of hypothermia.
ECG changes
Sinus bradycardia is followed by atrial flutter and fibrillation with ventricular ectopics. The PR interval, QRS complex, and QT interval are prolonged. Atrial activity eventually ceases. ‘J’ waves most often seen <31°C; ventricular fibrillation is common <30°C, with asystole <28°C.
Complications
Hypoxaemia is common due to hypoventilation and ventilation perfusion mismatch. Hypovolaemia and metabolic acidosis are common. Renal tubular damage may result from renal blood flow reduction. Acute pancreatitis, rhabdomyolysis, and gastric erosions are common.
Management
Oxygen to maintain SaO2 >95%.
Fluid replacement with careful monitoring.
Rewarming—all hypothermic patients with no evidence of other fatal disease should be assumed fully recoverable. In the event of cardiac arrest, full resuscitation should continue until normothermia is achieved. VF is resistant to defibrillation between 28–30°C. The technique used for rewarming depends on core temperature (measured with a low‐reading rectal thermometer) and clinical circumstances.
Rapid central rewarming
For core temperature <28°C (<33°C with acute exposure hypothermia) or where there is cardiac arrest, rapid rewarming should be instituted. This may be achieved by continous arterio‐venous rewarming circuits, peritoneal dialysis, gastric or bladder lavage with warmed fluids. Cardiopulmonary bypass is an effective rewarming strategy for patients with cardiac arrest resistant to defibrillation. These techniques may achieve rewarming rates of 1–5°C/h. Active surface rewarming with a heated blanket or warm air blanket can achieve rates of 1–7°C/h and is less invasive. Haemodynamic changes and fluid shifts may be dramatic during active rewarming, requiring careful monitoring and support. If extracorporeal rewarming is available, rates of 3–15°C/h may be achieved with the addition of cardiovascular support.
Spontaneous rewarming
Spontaneous rewarming proceeds at a rate inversely proportional to the duration of hypothermia. With good insulation (space blanket), rewarming rates of 0.1–0.7°C/h can be achieved. Core temperature may fall during spontaneous rewarming as cold blood is returned from the periphery to the central circulation.
Causes of hypothermia
Coma and immobility.
Cold water immersion.
Exposure.
Hypothyroidism.
Hypopituitarism.
Sepsis.
Erythroderma.
See also:
Pyrexia—causes
Pathophysiology
Mechanisms underlying temperature rise are poorly understood. It reflects the balance between heat loss and heat production. There may be inability to lose heat (e.g. high ambient temperature), ‘thermostat’ dysregulation within the hypothalamus, and increased heat generation (e.g. due to mitochondrial uncoupling). There is some laboratory evidence that a raised temperature may be beneficial in terms of white cell response, heat shock protein activation, and mitochondrial protection. Prognosis is worse in septic patients presenting with a low temperature.
An excessive temperature may be unpleasant to the patient (e.g. rigors). It will increase metabolic rate and therefore, oxygen demand, induce excessive vasodilatation, and increase salt and water loss. At very high temperatures, biochemical function is disrupted with altered enzyme function and increased cell breakdown (e.g. rhabdomyolysis).
Causes
Infection
The commonest cause in the ICU patient, though over‐diagnosed. Main sites are chest and intravascular catheter sites. Urinary tract infections are difficult to diagnose in the presence of a urethral catheter. Similarly, the respiratory tract is routinely colonised with bacteria within a few days of ICU admission; differentiation between colonising and pathogenic bacteria is difficult. Seek malaria in patients who have visited endemic areas. Antibiotic therapy may itself be a cause of pyrexia.
Inflammation
Inflammation unrelated to infection will usually generate a pyrexic response, e.g. systemic inflammatory response syndrome, post‐cardiac surgery, post‐burns, post‐myocardial infarction, vasculitis, glomerulonephritis, hepatitis, acalculous cholecystitis. Management is generally symptom‐orientated; this includes cooling.
Adverse drug reaction
Numerous drugs induce an idiosyncratic pyrexia, including antibiotics, sedatives, paralysing agents, and amphetamines. The neuroleptic malignant syndrome (NMS) is a rare, life‐threatening, idiosyncratic reaction to neuroleptics (e.g. haloperidol) and central dopamine blockers (e.g. metoclopramide). It is characterised by fever, muscular rigidity, altered mental status, and autonomic dysfunction. Usually, removal of the offending drug ± anti‐pyretics are sufficient, but more aggressive measures may have to be taken, including active cooling. Dantrolene is not recommended.
Adverse reaction to blood transfusion
May be an immunological reaction to a cellular constituent or contamination with an organism, bacterial cell product, or other pyrogen.
Ambient heating
Excessive heating or prevention of heat loss may cause pyrexia. Consider strong sunlight, temperature settings on specialised beds, and heat‐retaining clothing.
Miscellaneous
Other causes of pyrexia include neoplasm and cerebral insult.
Key paper
See also:
Pyrexia—management
At present, the optimal temperature to target in disease states is not known, other than cerebral insults where normo‐ or (preferably) hypothermia offers neuroprotection by reducing cerebral metabolic rate. In other conditions, it seems reasonable to accept mild pyrexia provided this is tolerated by the patient.
Principles of management
Diagnose, then remove or treat the offending cause. For example, seek and treat infection, stop blood infusion, and send discontinued bag to laboratory for analysis, discontinue administration of any causative drug, use anti‐inflammatory ± immunosuppressive agents for vasculitis.
Cooling aids symptomatic recovery, reduces metabolic rate, and lowers pressor requirements.
Increase evaporative losses, e.g. tepid sponging, wet sheets, ice packs in groin and axilla.
Increase convective losses, e.g. fanning to improve air circulation.
Cooled intravenous fluids.
Cooling blankets.
Antipyretics, e.g. paracetamol.
More aggressive cooling if temperature >41°C, e.g. irrigation of bladder/peritoneum with ice‐cool fluids, ice‐cool baths.
Aim to lower temperature <38.5°C, then reassess.
Paralysis and mechanical ventilation may be needed if the patient is shivering excessively.
Seek and treat concurrent rhabdomyolysis, DIC, seizures.
See also:
Hyperthermia
Hyperthermia is defined as a core temperature above 41°C.
Clinical features
Delirium and seizures are associated with temperatures of 40–42°C.
Coma is associated with temperatures >42°C.
Tachycardia.
Tachypnoea.
Salt and water depletion.
Rhabdomyolysis.
Disseminated intravascular coagulation.
Heart failure with ST depression and ‘T’ wave flattening.
Causes
Hyperthermia may be an extreme form of pyrogen‐induced fever associated with infection, inflammation, neoplasm, or CVA.
Heat stroke is associated with severe exercise in high environmental temperatures and humidity. Excess clothing, hypovolaemia, or recent alcohol intake reduces the body's ability to dissipate heat production.
Malignant hyperthermia is a drug‐induced myopathy associated with a hereditary calcium transfer defect in patients receiving volatile anaesthetics, muscle relaxants, antidepressants, alcohol, or Ecstasy. Heat production is increased by muscle catabolism, spasm, and peripheral vasoconstriction.
The neuroleptic malignant syndrome is a drug‐induced hyperthermic syndrome usually secondary to phenothiazines or butyrophenones. It is associated with muscle rigidity, akinesia, impaired consciousness, and autonomic dysfunction, and continues for 1–2 weeks.
Management
Institute rapid cooling for patients with temperatures >41°C.
Supportive treatment includes fluid replacement and seizure control.
Remove clothing and nurse in a cool environment.
Surface cooling can be achieved with a fan, tepid sponging, wet sheets, ice packs in groin and axillae, or a cool bath.
Handling should be minimised and active cooling measures should be stopped when the core temperature is <39°C.
Consider internal cooling using cooled IV fluid, and bladder lavage or peritoneal lavage using cooled fluids.
Phenothiazines may be used to reduce temperature and prevent shivering (do not give in neuroleptic malignant syndrome).
Consider muscle relaxants if the patient is ventilated.
For malignant hyperthermia, stop any offending drug.
Monitor and treat hyperkalaemia.
Treat the neuroleptic malignant syndrome by stopping the offending drug ± dopamine agonists (e.g. L‐dopa or bromocriptine). Dantrolene is no longer recommended as recovery is delayed and mortality may be increased.
See also:
Ventilatory support—indications, p44; Coagulation monitoring, p222; Basic resuscitation, p338; Heart failure—assessment, p392; Heart failure—management, p394; Coma, p438; Delirium, p442; Thyroid emergencies, p514; Amphetamines and ecstasy, p530; Pyrexia—causes, p602; Pyrexia—management, p604; Rhabdomyolysis, p612.
Electrocution
The effects of electrocution are due to the effects of the current and the conversion of electrical energy to heat energy on passage through the tissues. Important factors are:
Energy delivered—heat = amperage2 × resistance × time, i.e. the amperage is the most important determinant of heat production.
Resistance to current flow—tissues are resistant to current flow in the following decreasing order: bone, fat, tendon, skin, muscle, blood vessels, nerves. A high skin resistance and short duration of contact concentrate the effects locally. However, skin contaminants, moisture, and burning reduce resistance.
Type of current—alternating current is more dangerous than direct current. Tetanic muscle contractions may prevent the victim from releasing the current source whereas the single, strong muscle contraction with direct current often throws the victim clear. Alternating current is more likely to reach central tissues with consequent sustained apnoea and ventricular fibrillation (with as little as 50–100mA for 1–10ms).
Current pathway—cardiorespiratory arrest is more likely the closer the contact is with the chest and heart.
Lightening strike differs from contact electrocution in that high intensity, ultra‐short duration of current may produce cardiac arrest with little tissue destruction.
Clinical features
Tachyarrhythmias—including ventricular tachycardia and fibrillation.
Asystole—more likely with high current (>10A).
Myocardial injury—heat injury, coronary artery spasm, arrhythmias, myocardial spasm.
Respiratory arrest—tetanic contraction of the diaphragm, arrhythmias, cerebral medullary dysfunction.
Trauma—tetanic muscle contraction, falling or being thrown clear.
Burns—to skin and internal tissues.
Management
Most severe electrical injuries require urgent field treatment prior to hospital admission.
Ensure the source of the electrical injury is not a hazard to rescuers.
Manage cardiorespiratory arrest.
Prevent further injury, e.g. spinal protection, removal of smouldering clothes.
After hospital admission and restoration of the circulation, management is directed towards the complications.
Ventilatory support.
Management of hypovolaemia associated with burn injury. Fluid requirements are usually greater than for victims of thermal burns and require close monitoring.
Check cardiac enzymes for degree of myocardial injury. Treat heart failure and/or arrhythmias as indicated.
Management of rhabdomyolysis and covert compartment syndrome.
Surgical debridement of necrotic tissue and fixation of bony injury.
See also:
Near‐drowning
The major complications of near‐drowning are lung injury, hypothermia, and effects of prolonged hypoxia. Although hypothermia bestows protective effects against organ damage, rewarming carries particular hazards.
Pathophysiology
Prolonged immersion usually results in inhalation of fluid. However 10–20% of patients develop intense laryngospasm leading to so‐called ‘dry drowning’. Traditionally, fresh water drowning was considered to lead to rapid absorption of water into the circulation with haemolysis, hypo‐osmolality, and possible electrolyte disturbance whereas inhalation of hypertonic fluid from seawater drowning produced a marked flux of fluid into the alveoli. In practice, there seems to be little distinction between fresh and seawater as both cause loss of surfactant and severe inflammatory disruption of the alveolar‐capillary membrane leading to an ARDS‐type picture. Initially, haemodynamic instability is often minor. A similar picture often develops after ‘dry drowning’ and subsequent endotracheal intubation.
Acute hypothermia often accompanies near‐drowning with loss of consciousness and haemodynamic alterations.
Management
Oxygen—give sufficient to increase SaO2 >92%. Comatose patients should be intubated. Early CPAP or PEEP may be useful.
Bronchospasm is often present and may require nebulised B2 agonists, and either nebulised or SC epinephrine.
Fluid replacement should be directed by appropriate monitoring. Inotrope therapy may be necessary if hypoperfusion persists after adequate fluid resuscitation. Intravascular fluid overload is uncommon and the role of early diuretic therapy with a view to lowering intracranial pressure is controversial. Haemolysis may occur and require blood transfusion.
Arrhythmias may arise from myocardial hypoxia, hypothermia, and electrolyte abnormalities, and should be treated conventionally.
Metabolic acidosis may be profound. However, bicarbonate therapy is rarely indicated as the acidosis usually corrects on restoration of adequate tissue perfusion.
Electrolyte abnormalities are usually minor and can be managed conventionally.
Rewarming follows conventional practice; cardiopulmonary bypass may be considered if core temperature is <30°C. Cardiopulmonary resuscitation, including cardiac massage, should be continued until normo‐thermia is achieved.
Cerebral protection usually follows raised intracranial pressure protocols though, as mentioned above, the role of diuretic therapy and fluid restriction is controversial. Signs of brain damage such as seizures may become apparent and should be treated as they arise.
Antibiotic therapy (e.g. clindamycin or cefuroxime plus metronidazole) should be given if strong evidence of aspiration exists. Otherwise, take specimens and treat as indicated.
Decompress the stomach using a nasogastric tube to lessen any risk of aspiration. Enteral feeding can be initiated afterwards.
See also:
Endotracheal intubation, p42; Ventilatory support—indications, p44; Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68; Continuous positive airway pressure, p70; Bronchodilators, p254; Antiarrhythmics, p272; Basic resuscitation, p338; Cardiac arrest, p340; Hypothermia, p600.
Rhabdomyolysis
Breakdown of striated muscle that may result in compartment syndrome, acute renal failure, and electrolyte abnormalities (hyperkalaemia, hypocalcaemia, hyperphosphataemia).
Causes
Trauma, especially crush injury.
Prolonged immobilisation, e.g. after fall, drug overdose.
Drugs, e.g. opiates, cocaine, Ecstasy.
Hyperpyrexia.
Vascular occlusion (including lengthy vascular surgery).
Infection.
Burns/electrocution.
Severe hypophosphataemia.
Congenital myopathy (rare).
Diagnosis
Suggested by disproportionately high serum creatinine compared to urea (usual ratio is approximately 10 mol:1mmol).
Raised creatine kinase (usually >2000IU/L).
Myoglobinuria produces a positive urine dipstick to blood. Urine is usually red or black, but may be clear despite significant rhabdomyolysis.
General management
Admit for careful monitoring and adequate fluid resuscitation.
Do not treat hypocalcaemia unless the patient is symptomatic; calcium may form crystals with the high circulating phosphate.
Hyperkalaemia may be resistant to medical management and require urgent haemodialysis or haemodiafiltration.
Compartment syndrome
Suspect if limb is tender or extremely painful and peripheries are cool. Loss of peripheral pulses and tense muscles are late signs.
Manometry in muscle compartments reveal pressures >20–25mmHg.
Arm, legs, and buttock compartments may be affected.
Management involves either prophylactic fasciotomies if at high risk or close monitoring (including regular manometry) with decompression if pressures exceed 20–25mmHg.
Fasciotomies may result in major blood loss.
Renal failure
Renal failure is thought to be produced by a combination of free radical injury, hypovolaemia, hypotension, and possibly, myoglobin blocking the renal tubules.
Renal failure may be prevented by prompt rehydration and urinary alkalinisation with 1.26% sodium bicarbonate solution for 3–5 days. The urinary pH should be ≥6 and blood pH <7.5. Urinary alkalinisation increases urinary excretion of myoglobin.
Potassium, sodium, calcium, and magnesium levels should be monitored regularly and managed as appropriate.
If renal failure is established, dialysis, or filtration techniques will be required, usually for a period of 6–8 weeks.
Key paper
See also:
Haemo(dia)filtration (1), p108; Haemo(dia)filtration (2), p110; Urinalysis, p232; Sodium bicarbonate, p244; Oliguria, p398; Acute renal failure—diagnosis, p400; Acute renal failure—management, p402; Poisoning—general principles, p520; Salicylate poisoning, p522; Tricyclic antidepressant poisoning, p528; Amphetamines and ecstasy, p530; Multiple trauma (1), p582; Multiple trauma (2), p584; Hyperthermia, p606; Electrocution, p608.
Raised intra‐abdominal pressure
Intra‐abdominal pressure is normally <6mmHg at rest. A healthy individual may increase intra‐abdominal pressure to 25mmgHg with defaecation, 45mmHg with vomiting, and 60mmHg with coughing.
A sustained increase in intra‐abdominal pressure >15mmHg affects organs both within and outside the abdomen. The effects of raised intra‐abdominal pressure are known as the abdominal compartment syndrome. Left untreated, a raised intra‐abdominal pressure is associated with high mortality.
Transmission of pressure to the pleural space reduces lung compliance, altering the ventilation/perfusion ratio with resulting hypoxaemia and hypercapnia. Higher inspiratory pressures are required during mechanical ventilation. The resulting increase in both abdominal and intrathoracic pressures reduces venous return, leading to a fall in cardiac output and rise in intracranial pressure.
Despite the reduction in venous return, raised intra‐abdominal pressure will increase measured CVP. As a result of reduced cardiac output and venous congestion reducing capillary blood flow, perfusion of the intra‐abdominal organs is reduced. Oliguria and renal failure, splanchnic hypoperfusion, and decreased liver metabolism may result.
Causes
Bowel or abdominal wall oedema, e.g. large volume resuscitation.
Intestinal obstruction.
Intra‐ and retroperitoneal haemorrhage, e.g. ruptured aneurysm.
Morbid obesity.
Ascites.
Peritoneal dialysis.
Measuring intra‐abdominal pressure
The classical technique is to measure pressure in the relaxed bladder via a Foley catheter. With the patient supine, the catheter tubing is clamped distal to the sampling bung. A pressure manometer is connected to a three‐way tap and needle which is inserted into the sampling bung. The bladder should be partially filled via the three‐way tap with 50mL 0.9% saline. The transducer should then be zeroed at the level of the symphysis pubis. The bladder pressure measurement is assumed to be equivalent to intra‐abdominal pressure. Manometers for measuring the bladder pressure are now available commercially.
Management
Removal of cause if possible.
Restoration of cardiac output with fluid resuscitation.
Consider surgical decompression (laparostomy) or tube decompression for pseudo‐obstruction if intra‐abdominal pressure >25mmHg.
See also:
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