Adapted from Mount Vernon formula \200 Divide \201 rst 36h from the time of burn into six consecutive periods of 4, 4, 4, 6, 6, and 12h. For each period, give 0.5mL 5% albumin \227 bodyweight [kg] \227 % burn. Give 1. 5 \200\2232mL/kg/h 5% glucose. \200 With either formula, give blood as necessary to maintain Hb >10g/dL. Reassess cardiorespira tory variables and urine output at frequent intervals to determine whether volume replaceme nt is inadequate or excessive; adjust \202 uid input accordingly. See also: Central venous catheter \200\224use, p170; Pulmonary artery catheter \200\224use, p176; Cardiac output \200\224 central thermodilution, p178; Cardiac output \200\224periphe ral thermodilution, p180; Cardiac output \200\224 indicator dilution, p182; Cardiac output \200\224Doppler ultrasound, p184; Cardiac output \200\224pulse contour analysis, p186; Card iac output \200\224other techniques, p188; Pressure and stroke volume vari- ation, p190; Cr ystalloids, p242; Colloids, p246; Blood transfusion, p248; Basic resuscitation, p338; Fluid challenge, p342; Burns \200\224general management, p594. 594 CHAPTER 32 Trauma and burns Burns \200\224general management Surgery \200 Escharotomy may be needed on hospital admission to affected limbs as well as the neck and/o r chest if a circumferential burn is present. Debridement of necrotic tissue is often begun within the \201 rst few days as early grafting is associated with improved outcome. Cove rage is obtained using either split skin grafts from the patient \200\231s own unaffected s kin, donor skin grafts, or even experimental \200\230skin \200\231. Blood loss may be rapi d and massive, e.g. 100mL per 1% of body surface grafted. Wound care \200 Early application of dressings and Flamazine (silver sulphadiazine) cream, which has antiba cterial properties against Gram-negative bacteria, may usefully prevent secondary infection . Early grafting often takes place within the \201 rst 2 \200\2233 days to provide a skin protective barrier. Nutrition \200 Enteral nutrition should be commenced soon after admission as studies have shown that early enteral nutrition improves outcome. Target intake is protein of 1g/kg + 2g per % burn, and a calorie intake of 20Cal/kg + 50Cal per % burn. Infection \200 \200 Prophylactic antibiotics are often not given to burn patients. Body temperature rises on da ys 1 \200\2232 as high as 40*C may persist for several days and does not indicate secondary infection. Likely infecting agents include Streptococci, Staphylococci, and Gram- negative bacteria such as Pseudomonas. Appropriate antibiotic treatment should be given as indicate d. Other considerations \200 \200 Diagnose and treat any suspected inhalation injury. Ensure adequate analgesia (opiates). Ke tamine is a useful anesthetic as it also has analgesic properties. Tetanus toxoid should be given soon after hospital admission. Reduce heat and \202 uid losses by placing the pati ent on a heated air- \202 uidised bed and by early coverage of burnt skin through applica tion of occlusive dressings and placing affected limbs in transparent plastic bags. Stress ulceration can usually be avoided through prompt resuscitation and early enteral nutrition. Prevent pressure sores and contractures by careful nursing and physiotherapy. Avoid suxame thonium from 5 \200\223150 days post-burn because of the risk of rapid and severe hyperkala emia. Increasing resistance to non-depolarising muscle relaxants may occur. B-blockade has been associated with outcome improvement in children sustaining burn injury. \200 \200 BURNS \200\224GENERAL MANAGEMENT 595 See also: Enteral nutrition, p128; Wound and pressure sore management, p136; Wound manageme nt princi- ples, p136; Dressing techniques, p138; Special support surfaces, p140; Non-opioi d analgesics, p302; Opioid analgesics, p304; Infection control \200\224general principles, p544; Infection \200\224diagnosis, p552; Infection \200\224treatment, p554; Systemic in \202 ammation/multi-organ failure \200\224causes, p556; Burns \200\224 \202 uid management , p592. 596 CHAPTER 32 Trauma and burns Blast injury Pathophysiology Blast injuries are traditionally divided into four categories: primary, secondary, tertiary, and quaternary (or miscellaneous) injuries. \200 Primary blast injury is caused by the direct effect of blast overpressure on tissue. Unlike water, air is easily compressible so air- \201 lled structures such as lung, ear, and the gastrointestinal tract are frequently affected. Tympanic membrane rupture indicates high-p ressure wave ( \211 40kPa) injury and suggests (but does not con \201 rm) the presence of vital organ injury. Secondary blast injury is ballistic trauma related to \202 ying objec ts. The severity of a ballistic wound is determined by the kinetic energy of the projectile . Therefore, velocity has more impact than mass of the object. Tertiary blast injury occurs with high-energy explosions when people \202 y through the air and strike other objects. Quaternary injuries cover all other injuries, e.g. burns, crush injuries, and toxic gas/sm oke inhalation. Investigations (as indicated) Assessment should be as for any trauma with focus on airway, breathing, and circulation followed by a primary assessment of injuries. \200 Lung \200\224X-ray or CT scan for lung contusion, pneumothorax, ARDS, \202 ail chest. Con tusion may evolve over several hours. Heart \200\224ECG, echocardiography, and troponin for myocardial contusion and to exclude pericardial tamponade. Abdomen \200\224CT scan to excl ude injury to both solid and hollow organs, including penetrating objects, perforation, cav itation, and occult hemorrhage. Intestinal haematoma can take up to 36h to develop. Intesti nal perforation is more common with underwater blast injury. X-ray or CT to other injured a reas \200\224for fractures, shrapnel, gas embolus, etc. Blood tests for diagnosis of DIC, r habdomyolysis. Management \200 \200 Standard surgical management of fractures, burns, wounds, etc. If possible, avoid positive pressure ventilation and PEEP due to the risk of alveolar rupture and air embolus. If IPPV is necessary, use low tidal volumes and minimize airway pressure. For patients with arteria l gas embolism (AGE), give 100% O2 by tight- \201 tting face mask, and if possible, place the patient in the left lateral position to minimize risk of further air emboli leaving th e heart. If the lung responsible for the air emboli can be identi \201 ed, single lung ven tilation may prevent further air entry into the vasculature during IPPV. Hyperbaric oxygen treatment is the de \201 nitive treatment for AGE, especially cerebral AGE where blood ves sels in brain or spinal cord are occluded. Myocardial depression usually self-reverses with in minutes to hours. Consider and treat as appropriate: (i) DIC, (ii) carbon monoxide, smok e and other toxic inhalation, (iii) rhabdomyolysis and compartment syndrome, and (iv) perip heral compression injuries. Follow local protocols for biological, chemical, or radiation c ontamination if a \200\230dirty \200\231 bomb is implicated in the blast injury. \200 BLAST INJURY 597 See also: Respiratory imaging, p158; ECG monitoring, p162; Echocardiography, p192; Cardiac function tests, p216; Pneumothorax, p368; Inhalation injury, p374; Multiple trauma (1), p58 2; Multiple trauma (2), p584; Rhabdomyolysis, p612; Raised intra-abdominal pressure, p614. This page intentionally left blank 599 Chapter 33 Physical disorders Hypothermia 600 Pyrexia \200\224causes 602 Pyrexia \200\224management 604 Hyperthermia 606 Electrocution 608 Near-drowning 610 Rhabdomyolysis 612 Raised intra-abdominal pressure 614 600 CHAPTER 33 Physical disorders Hypothermia Clinical features \200 \200 \200 >33*C \200\224shivering in an attempt to correct body temperature. <33*C \200\224neurologic al signs of dysarthria and slowness appear. <31*C \200\224hypertonicity and sluggish re \202 exes with cardiovascular dysfunction become life-threatening. <28*C \200\224arterial p ulses often impalpable. Hypothermic rigidity is dif \201 cult to distinguish from death. Prognosis depends on the degree and duration of hypothermia. ECG changes Sinus bradycardia is followed by atrial \202 utter and \201 brillation with ventric- ular ectopics. The PR interval, QRS complex, and QT interval are pro- longed. Atr ial activity eventually ceases. \200\230J \200\231 waves most often seen <31*C; ventricula r \201 brillation is common <30*C, with asystole <28*C. Complications Hypoxaemia is common due to hypoventilation and ventilation perfusion mismatc h. Hypovolaemia and metabolic acidosis are common. Renal tubular damage may result from ren al blood \202 ow reduction. Acute pan- creatitis, rhabdomyolysis, and gastric erosions ar e common. Management 1. Oxygen to maintain SaO2 >95%. 2. Fluid replacement with careful monitoring. 3 . Rewarming \200\224all hypothermic patients with no evidence of other fatal disease should be assumed fully recoverable. In the event of cardiac ar- rest, full resuscitation should continue until normothermia is achieved. VF is resistant to de \201 brillation between 28 \200\22330*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 achieve d by continous arterio-venous rewarming circuits, perito- neal dialysis, gastric or bladder lavage with warmed \202 uids. Cardiopulmonary bypass is an effective rewarming strategy for patients with cardiac arrest resistant to de \201 brillation. These techniques may ach ieve rewarming rates of 1 \200\2235*C/h. Active surface rewarming with a heated blanket or warm air blanket can achieve rates of 1 \200\2237*C/h and is less invasive. Haemodynamic ch anges and \202 uid shifts may be dramatic during active rewarming, requiring careful moni toring and support. If extracorporeal rewarming is available, rates of 3 \200\22315*C/h may be achieved with the addition of cardiovascular support. Spontaneous rewarming Spontaneous rewarming proceeds at a rate inversely proportional to th e duration of hypothermia. With good insulation (space blanket), rewarming rates of 0.1 \200\2230.7*C/h can be achieved. Core temperature may fall during spontaneous rewarming as cold blood is returned from the periphery to the central circulation. HYPOTHERMIA 601 Causes of hypothermia \200 Coma and immobility. \200 Cold water immersion. \200 Expos ure. \200 Hypothyroidism. \200 Hypopituitarism. \200 Sepsis. \200 Erythroderma. See also: Electrical cardioversion, p94; ECG monitoring, p162; Basic resuscitation, p338; C ardiac arrest, p340; Tachyarrhythmias, p384; Bradyarrhythmias, p386; Pancreatitis, p424; Th yroid emergencies, p514; Rhabdomyolysis, p612. 602 CHAPTER 33 Physical disorders Pyrexia \200\224causes Pathophysiology Mechanisms underlying temperature rise are poorly un derstood. It re \202 ects the balance between heat loss and heat production. There may be inability to lose heat (e.g. high ambient temperature), \200\230thermostat \200\231 dysreg ulation within the hypothalamus, and increased heat generation (e.g. due to mito- chondrial uncoupling). There is some laboratory evidence that a raised temperature may be bene \201 cial in terms of white cell response, heat shock protein activation, and mitochondrial pro tection. 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 m etabolic rate and therefore, oxygen demand, induce excessive vasodilatation, and increase s alt and water loss. At very high temperatures, biochemical function is disrupted with alter ed enzyme func- tion 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 dif \201 cult to diagnose in the presence of a urethral catheter. Similarly, the respiratory tract is routin ely colonized with bacteria within a few days of ICU admission; differentiation between col onizing and pathogenic bac- teria is dif \201 cult. Seek malaria in patients who have visi ted endemic areas. Antibiotic therapy may itself be a cause of pyrexia. In \202 ammation I n \202 ammation unrelated to infection will usually generate a pyrexic response, e.g. syst emic in \202 ammatory response syndrome, post-cardiac surgery, post-burns, post-myocardial infarction, vasculitis, glomerulonephritis, hepatitis, acalculous cholecystitis. Managemen t is generally symptom- orientated; this includes cooling. Adverse drug reaction Numerous d rugs induce an idiosyncratic pyrexia, including antibiotics, sedatives, paralyzing agents, and amphetamines. The neuroleptic malig- nant syndrome (NMS) is a rare, life-threatening, i diosyncratic reaction to neuroleptics (e.g. haloperidol) and central dopamine blockers (e.g . meto- clopramide). It is characterized by fever, muscular rigidity, altered mental status , and autonomic dysfunction. Usually, removal of the offending drug 9 anti-pyretics are suf \201 cient, but more aggressive measures may have to be taken, including active cooling. Dantrolene is not recommended. Adverse reaction to blood transfusion May be an immunologica l reaction to a cellular constituent or contamina- tion with an organism, bacterial cell pr oduct, or other pyrogen. Ambient heating Excessive heating or prevention of heat loss may c ause pyrexia. Consider strong sunlight, temperature settings on specialized beds, and heat- retaining clothing. Miscellaneous Other causes of pyrexia include neoplasm and cerebral in sult. PYREXIA \200\224CAUSES 603 Key paper Circiumaru B, Baldock G, Cohen J. (1999) A prospective study of fever in the inte nsive care unit. Intensive Care Med 25: 668 \200\22373. See also: Blood transfusion, p248; Blood products, p250; Generalized seizures, p444; Stroke , p452; Infection \200\224diagnosis, p552; Systemic in \202 ammation/multi-organ failure \200\224causes, p556; Head injury (1), p586; Head injury (2), p588. 604 CHAPTER 33 Physical disorders Pyrexia \200\224management At present, the optimal temperature to target in disease states is not known, other than cerebral insults where normo- or (preferably) hypo- thermia offers neuroprotection by reducing cerebral metabolic rate. In other conditions, it seems reasona ble to accept mild pyrexia provided this is tolerated by the patient. Principles of management 1. Diagnose, then remove or treat the offending cause. For example , seek and treat infection, stop blood infusion, and send discontinued bag to laboratory fo r analysis, discontinue administration of any causative drug, use anti-in \202 ammatory 9 immunosuppressive agents for vasculitis. 2. Cooling aids symptomatic recovery, reduces meta bolic rate, and lowers pressor requirements. \200 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 \202 uids. Cooling blankets. Antipyretics, e.g. paracetamol. More aggressive cooling if te mperature >41*C, e.g. irrigation of bladder/peritoneum with ice-cool \202 uids, ice-cool baths. Aim to lower temperature <38.5*C, then reassess. \200 \200 \200 \200 3. Paralysis and mechanical ventilation may be needed if the patient is shivering excessively. 4. Seek and treat concurrent rhabdomyolysis, DIC, seizures. PYREXIA \200\224MANAGEMENT 605 See also: Therapeutic hypothermia, p100; Infection \200\224treatment, p554 Sepsis and septi c shock \200\224treatment, p560; Pyrexia \200\224causes, p602. 606 CHAPTER 33 Physical disorders Hyperthermia Hyperthermia is de \201 ned as a core temperature above 41*C. Clinical features \200 \200 \200 \200 \200 \200 \200 \200 Delirium and seizures are associated with temperatures of 40 \200\22342*C. Coma is associat ed with temperatures >42*C. Tachycardia. Tachypnoea. Salt and water depletion. Rhabdomyolys is. Disseminated intravascular coagulation. Heart failure with ST depression and \200\230T \200\231 wave \202 attening. Causes \200 Hyperthermia may be an extreme form of pyrogen-induced fever associated with infection, in \202 ammation, neoplasm, or CVA. Heat stroke is associated with severe exercise in high en vironmental temperatures and humidity. Excess clothing, hypovolaemia, or recent alcohol int ake reduces the body \200\231s ability to dissipate heat production. Malignant hyperthermia is a drug-induced myopathy associated with a hereditary calcium transfer defect in patient s receiving volatile anesthetics, muscle relaxants, antidepressants, alcohol, or Ecstasy. H eat production is increased by muscle catabolism, spasm, and peripheral vasoconstriction. T he neuroleptic malignant syndrome is a drug-induced hyperthermic syndrome usually secondary to phenothiazines or butyrophenones. It is associated with muscle rigidity, akinesia, impa ired consciousness, and autonomic dysfunction, and continues for 1 \200\2232 weeks. Management 1. Institute rapid cooling for patients with temperatures >41*C. 2. Supportive t reatment includes \202 uid replacement and seizure control. 3. Remove clothing and nurse in a cool environment. 4. Surface cooling can be achieved with a fan, tepid sponging, wet s heets, ice packs in groin and axillae, or a cool bath. 5. Handling should be minimized and active cooling measures should be stopped when the core temperature is <39*C. 6. Consider internal cooling using cooled IV \202 uid, and bladder lavage or peritoneal lavage using cooled \202 uids. 7. Phenothiazines may be used to reduce temperature and prevent shiv- ering (do not give in neuroleptic malignant syndrome). 8. Consider muscle relaxants if the patient is ventilated. 9. For malignant hyperthermia, stop any offending drug. 10. Monitor and treat hyperkalaemia. 11. Treat the neuroleptic malignant syndrome by stopping the offen ding drug 9 dopamine agonists (e.g. L-dopa or bromocriptine). Dantrolene is no longer recom mended as recovery is delayed and mortality may be increased. HYPERTHERMIA 607 See also: Ventilatory support \200\224indications, p44; Coagulation monitoring, p222; Basic resuscitation, p338; Heart failure \200\224assessment, p392; Heart failure \200\224managem ent, p394; Coma, p438; Delirium, p442; Thyroid emergencies, p514; Amphetamines and ecstasy, p530; Pyrexia \200\224causes, p602; Pyrexia \200\224 management, p604; Rhabdomyolysis, p61 2. 608 CHAPTER 33 Physical disorders Electrocution The effects of electrocution are due to the effects of the current and the co nversion of electrical energy to heat energy on passage through the tissues. Important fact ors are: \200 Energy delivered \200\224heat = amperage2 x resistance x time, i.e. the amperage is the mos t important determinant of heat production. Resistance to current \202 ow \200\224tissues are resistant to current \202 ow in the following decreasing order: bone, fat, tendon, s kin, muscle, blood vessels, nerves. A high skin resistance and short duration of contact co ncentrate the effects locally. However, skin contaminants, moisture, and burning reduce res istance. Type of current \200\224alternating current is more dangerous than direct current. Tetanic muscle contractions may prevent the victim from releasing the current source where as 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 apno ea and ventricular \201 brillation (with as little as 50 \200\223100mA for 1 \200\22310ms ). Current pathway \200\224cardiorespiratory arrest is more likely the closer the contact i s with the chest and heart. Lightening strike differs from contact electrocution in that high intensity, ultra-short du ration of current may produce cardiac arrest with little tissue destruction. Clinical features \200 \200 \200 Tachyarrhythmias \200\224including ventricular tachycardia and \201 brillation. Asystole \200\224more likely with high current (>10A). Myocardial injury \200\224heat injury, corona ry artery spasm, arrhythmias, myocardial spasm. Respiratory arrest \200\224tetanic contract ion of the diaphragm, arrhythmias, cerebral medullary dysfunction. Trauma \200\224tetanic m uscle contraction, falling or being thrown clear. Burns \200\224to skin and internal tissue s. \200 Management Most severe electrical injuries require urgent \201 eld treatment prior to hos - pital admission. 1. Ensure the source of the electrical injury is not a hazard to rescuer s. 2. Manage cardiorespiratory arrest. 3. Prevent further injury, e.g. spinal protection, r emoval of smoldering clothes. After hospital admission and restoration of the circulation, management is directed towards the complications. 1. Ventilatory support. 2. Management of hypovolaemia associated with b urn injury. Fluid re- quirements are usually greater than for victims of thermal burns and require close monitoring. 3. Check cardiac enzymes for degree of myocardial injury. Treat heart failure and/or arrhythmias as indicated. 4. Management of rhabdomyolysis and covert compartment syndrome. 5. Surgical debridement of necrotic tissue and \201 xation of bony injury. ELECTROCUTION 609 See also: Endotracheal intubation, p42; Ventilatory support \200\224indications, p44; Elect rical cardioversion, p94; Cardiac function tests, p216; Basic resuscitation, p338; Cardiac arrest, p340; Tachyarrhythmias, p384; Burns \200\224 \202 uid management, p592; Burns \200 \224general management, p594; Rhabdomyolysis, p612. 610 CHAPTER 33 Physical disorders Near-drowning The major complications of near-drowning are lung injury, hypothermia, and ef fects of prolonged hypoxia. Although hypothermia bestows protec- tive effects against organ damage, rewarming carries particular hazards. Pathophysiology Prolonged immersion usually results in inhalation of \202 uid. However 10 \200\223 20% of patients develop intense laryngospasm leading to so-called \200\230dry dr owning \200\231. Traditionally, fresh water drowning was considered to lead to rapid absorp tion of water into the circulation with haemolysis, hypo-osmo- lality, and possible electro lyte disturbance whereas inhalation of hypertonic \202 uid from seawater drowning produce d a marked \202 ux of \202 uid into the alveoli. In practice, there seems to be little distinction between fresh and seawater as both cause loss of surfactant and severe in \202 ammatory disrup- tion of the alveolar-capillary membrane leading to an ARDS-type picture. Initially, haemodynamic instability is often minor. A similar picture often develops after \200\230dry drowning \200\231 and subsequent endotracheal intubation. Acute hypothermia often accompanies near-drowning with loss of con- sciousness and haemodynamic alterations. Management 1. Oxygen \200\224give suf \201 cient to increase SaO2 >92%. Comatose patients should be intubated. Early CPAP or PEEP may be useful. 2. Bronchospasm is often present and may require nebulised B2 agonists, and either nebulised or SC epinephrine. 3. Fluid replacement should be directed by appropriate monitoring. Inotrope therapy may be necessary if hypoperfusion persists after adequate \202 uid resuscitation. Intravascular \202 uid overload is uncommon and the role of early diuretic therapy with a view to lower ing intracra- nial pressure is controversial. Haemolysis may occur and require blood transf usion. 4. Arrhythmias may arise from myocardial hypoxia, hypothermia, and electrolyte abnormalities, and should be treated conventionally. 5. Metabolic acidosis may be profound. However, bicarbonate therapy is rarely indicated as the acidosis usually corrects on restoration of adequate tissue perfusion. 6. Electrolyte abnormalities are usually minor and can be managed con- ventionally. 7. Rewarming follows conventional practice; cardiopulmonary bypass may be considered if cor e temperature is <30*C. Cardiopulmonary resuscitation, including cardiac massage, should be continued until normo-thermia is achieved. 8. Cerebral protection usually follows raised intracranial pressure proto- cols though, as mentioned above, the role of diuretic therapy and \202 uid restriction is controversial. Signs of brain damage such as seizures may become apparent and should be treated as they ar ise. 9. Antibiotic therapy (e.g. clindamycin or cefuroxime plus metronidazole) should be given i f strong evidence of aspiration exists. Otherwise, take specimens and treat as indicated. 10. Decompress the stomach using a nasogastric tube to lessen any risk of aspiration. Enteral feeding can be initiated afterwards. NEAR-DROWNING 611 See also: Endotracheal intubation, p42; Ventilatory support \200\224indications, p44; Posit ive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68; Continuous positive airway pressure, p70; Bronchodilators, p254; Antiarrhythmics, p272; Basic resusci tation, p338; Cardiac arrest, p340; Hypothermia, p600. 612 CHAPTER 33 Physical disorders Rhabdomyolysis Breakdown of striated muscle that may result in compartment syndrome, acute renal failure, and electrolyte abnormalities (hyperkalaemia, hypocal- caemia, hyperphosphat aemia). Causes \200 \200 \200 \200 \200 \200 \200 \200 \200 Trauma, especially crush injury. Prolonged immobilization, 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 myo pathy (rare). Diagnosis \200 Suggested by disproportionately high serum creatinine compared to urea (usual ratio is appr oximately 10 mol:1mmol). Raised creatine kinase (usually >2000IU/L). Myoglobinuria produce s a positive urine dipstick to blood. Urine is usually red or black, but may be clear despi te signi \201 cant rhabdomyolysis. \200 General management \200 \200 Admit for careful monitoring and adequate \202 uid resuscitation. Do not treat hypocalcae mia unless the patient is symptomatic; calcium may form crystals with the high circulating phosphate. Hyperkalaemia may be resistant to medical management and require urgent haemodia lysis or haemodia \201 ltration. Compartment syndrome \200 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 \200\22325mmHg. Arm, legs, and buttock compartments may be affected. Management involv es either prophylactic fasciotomies if at high risk or close monitoring (including regular manometry) with decompression if pressures exceed 20 \200\22325mmHg. Fasciotomies may resul t in major blood loss. \200 \200 Renal failure \200 Renal failure is thought to be produced by a combination of free radical injury, hypovolaem ia, hypotension, and possibly, myoglobin blocking the renal tubules. Renal failure may be p revented by prompt rehydration and urinary alkalinisation with 1.26% sodium bicarbonate sol ution for 3 \200\2235 days. The urinary pH should be \211 6 and blood pH <7.5. Urinary alk alinisation increases urinary excretion of myoglobin. Potassium, sodium, calcium, and magne sium levels should be monitored regularly and managed as appropriate. If renal failure is e stablished, dialysis, or \201 ltration techniques will be required, usually for a period of 6 \200\2238 weeks. RHABDOMYOLYSIS 613 Key paper Better OS, Stein JH. (1990) Early management of shock and prophylaxis of acute re nal failure in traumatic rhabdomyolysis. N Engl J Med 322: 825 \200\2239. See also: Haemo(dia) \201 ltration (1), p108; Haemo(dia) \201 ltration (2), p110; Urinaly sis, p232; Sodium bicarbo- nate, p244; Oliguria, p398; Acute renal failure \200\224diagnosi s, p400; Acute renal failure \200\224management, p402; Poisoning \200\224general 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. 614 CHAPTER 33 Physical disorders Raised intra-abdominal pressure Intra-abdominal pressure is normally <6mmHg at rest. A heal thy individual may increase intra-abdominal pressure to 25mmgHg with defaecation, 45mmHg wi th vomiting, and 60mmHg with coughing. A sustained increase in intra-abdominal pressure >15mmHg affects organs both within and out side the abdomen. The effects of raised intra- abdominal pressure are known as the abdomina l compartment syndrome. Left untreated, a raised intra-abdominal pressure is associated wit h high mortality. Transmission of pressure to the pleural space reduces lung compliance, altering the ventila tion/perfusion ratio with resulting hypoxaemia and hypercapnia. Higher inspiratory pressure s 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 measu red CVP. As a result of reduced cardiac output and venous congestion reducing capillary blo od \202 ow, perfusion of the intra- abdominal organs is reduced. Oliguria and renal failu re, splanchnic hypop- erfusion, and decreased liver metabolism may result. Causes \200 \200 \200 \200 \200 \200 Bowel or abdominal wall oedema, e.g. large volume resuscitation. Intestinal obstruction. In tra- and retroperitoneal hemorrhage, e.g. ruptured aneurysm. Morbid obesity. Ascites. Perit oneal dialysis. Measuring intra-abdominal pressure The classical technique is to measure pressure in the re laxed 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 need le which is inserted into the sampling bung. The bladder should be partially \201 lled vi a the three-way tap with 50mL 0.9% saline. The transducer should then be zeroed at the leve l of the symphysis pubis. The bladder pressure measurement is assumed to be equivalent to i ntra-abdominal pressure. Manometers for measuring the bladder pres- sure are now available commercially. Management \200 \200 \200 Removal of cause if possible. Restoration of cardiac output with \202 uid resuscitation. Consider surgical decompression (laparostomy) or tube decompression for pseudo-obstruction if intra-abdominal pressure >25mmHg. RAISED INTRA-ABDOMINAL PRESSURE 615 See also: IPPV \200\224failure to deliver ventilation, p54; Respiratory failure, p350; Olig uria, p398; Acute renal failure \200\224diagnosis, p400; Intra-abdominal bowel perforation and obstruction, p418; Abdominal sepsis, p422; Pancreatitis, p424; Rhabdomyolysis, p612. This page intentionally left blank 617 Chapter 34 Pain and post-operative critical care Pain 618 Post-operative critical care 620 618 CHAPTER 34 Pain and post-operative critical care Pain Pain results from many insults, e.g. trauma, invasive procedures, speci \201 c organ disease, and in \202 ammatory processes. Pain relief is necessary for physiological and ps ychological reasons: \200 \200 Anxiety and lack of sleep. Increased sympathetic activity contributing to an increased meta bolic demand and adrenergic stress. The capacity of the circulation and respiratory system to meet this increase in metabolic demand may not be adequate. Myocardial ischaemia is a si gni \201 cant risk. The endocrine response to injury is exaggerated with consequent salt a nd water retention. Physiological attempts to limit pain may include immobility and muscle splinting, and consequent reductions in ventilatory function and cough. \200 Pain perception The degree of tissue damage is related to the magnitude of the pain stim- u lus. The site of injury is also important; thoracic and upper abdominal injury is more pain ful than injury elsewhere. However, the perception of pain is dependent on other factors, e .g. simultanous sensory input, per- sonality, cultural background, and previous experiences of pain. Management of pain Systemic analgesia \200 \200 Opioid analgesics form the mainstay of analgesic drug treatment. Small, frequent IV doses, or a continuous infusion provide the most stable blood levels. Since the degree of analgesi a is dependent on blood levels, it is important that they are maintained. Higher doses are required to treat rather than prevent pain. The dose of drug required for a particular indi vidual depends on their perception of pain and whether tolerance has built up to previous a nalgesic use. The use of non-opioid drugs may avoid the need for or reduce the dose require d of opioid drugs. This includes paracetamol and non- steroidals, ketamine, and A2-agonists such as clonidine. \200 Regional analgesia \200 Regional techniques reduce respiratory depression, but require experience to ensure procedu res are performed safely. Epidural analgesia may be with local anesthetic agents or opioids . Opioids avoid the vasodilatation and hypotension associated with local anesthetic agents, but do not produce as profound analgesia. The combination of opioid and local anesthetic i s synergistic. Intravenous opioids should be avoided or close monitoring should continue fo r 24h after cessation of epidural opioids due to the potential for late respiratory failure . Sample regimens are shown opposite. Local anesthetic agents may be used to block super \201 cial nerves, e.g. intercostal nerve block with 3 \200\2235mL 0.5% bupivacaine plus adr enaline. \200 \200 Non-pharmacological techniques Adequate explanation, positioning and physical techniques ma y all reduce drug requirements. PAIN 619 Regimens for epidural analgesia Lumbar 10 \200\22315mL 0.5% bupivacaine, followed by an infusion of 5 \200\22320mL/h 0.125% bupiva caine Thoracic 4 \200\2236mL 0.5% bupivacaine followed by an infusion of 6 \200\22310mL/h 0.125% bupivacai ne Opioid 5mg morphine gives up to 12h analgesia. Combined An infusion of 3 \200\2234mL/h 0.125% bupivacaine with 0.3 \200\2230.4mg/h morphine or 25 \200\22350mcg/h fentanyl See also: Non-opioid analgesics, p302; Opioid analgesics, p304; Epidural analgesia, p306; M ultiple trauma (2), p584; Blast injury, p596; Post-operative critical care, p620; Pain and comfort, p624. 620 CHAPTER 34 Pain and post-operative critical care Post-operative critical care Patients may be admitted to critical care after surgery, eithe r electively (see table opposite) or after unexpected peri-operative complications. General care \200 Ensure surgical and anesthetic plan has been agreed, e.g. overnight ventilation, special pr ecautions (e.g. wire cutters if mandible wired), movement restriction, haemodynamic targets , etc. Provide adequate analgesia. Ensure adequate rewarming. Maintain euglycaemia. Provide appropriate thrombosis prophylaxis. Blood gas, electrolyte, and hemoglobin monitoring. \200 \200 \200 \200 Post-operative respiratory problems Common in those with pre-existing respiratory disease, especially with a reduced vital capacity or peak \202 ow rate. Problems include: \200 \200 \200 \200 \200 Exacerbation of chronic chest disease. Retained secretions. Basal atelectasis. Pneumonia. U pper airway problems, e.g. laryngeal oedema. Anesthesia and surgery (especially upper abdominal surgery) reduce functional residual capa city, thoracic compliance, and cough. There is reduced macrophage function and systemic in \202 ammatory activation with infection and acute lung injury as possible consequences. Therapeutic aims Preoperative preparation may help avoid some of the problems: \200 \200 \200 \200 \200 Cessation of smoking for >1 week. Bronchodilatation. Respiratory muscle training. Chest phy siotherapy. Avoidance of hypovolaemia in the nil-by-mouth period. Post-operative clearance of secretions and maintenance of basal lung expansion are very imp ortant. These require effective analgesia and chest physiotherapy. Mechanical ventilation a ssists basal expansion and secre- tion clearance where anesthetic recovery is expected to b e prolonged or surgery 9 pre-existing disease increases the risk of secretion retention and atelectasis. Ensure a patent airway prior to extubation. Post-operative circulatory proble ms \200 Prevention of hypovolaemia is crucial in avoiding in \202 ammatory activation and, therefo re, many post-operative complications. Hemorrhage is usually obvious and managed by resusci tation, correction of coagulation disturbance, and surgery. Sub-clinical hypovolaemia is co mmon. Hypothermia and high catecholamine levels help to maintain CVP and BP despite continu ing hypovolaemia. Avoiding a reduced stroke volume, metabolic acidosis, and a low ScvO2 are the best indicators of adequate resuscitation. Fluid challenges with colloid should be use d to con \201 rm and treat hypovolaemia where there is any circulatory disturbance, metabo lic acidosis, or oliguria. POST-OPERATIVE CRITICAL CARE 621 Reasons for elective critical care admission \200 \200 Airway monitoring, e.g. major oral, head, and neck surgery. Respiratory monitoring, e.g. ca rdiothoracic surgery, upper abdominal surgery, prolonged anesthesia, previous respiratory d isease. Cardiovascular monitoring, e.g. cardiac surgery, vascular surgery, major abdominal surgery, prolonged anesthesia, previous cardiovascular disease. Neurological monitoring, e. g. neurosurgery, cardiac surgery with circulatory arrest, spinal surgery. Flap monitoring, e.g. major plastic, and head and neck surgical procedures. Elective ventilation, e.g. cardi ac surgery, major abdominal surgery, prolonged anesthesia, previous respiratory disease. See also: Critical Care Unit admission criteria, p10; Oxygen therapy, p38; Airway maintenan ce, p40; Ventilatory support \200\224indications, p44; Continuous positive airway pressure, p70; Non-invasive respiratory support, p76; Chest physiotherapy, p90; Blood transfusion, p 248; Fluid challenge, p342; Airway obstruction, p348; Respiratory failure, p350; Atelectasi s and pulmonary collapse, p352; Hypotension, p380; Oliguria, p398; Vomiting/gastric stasis, p406; Abdominal sepsis, p422; Bleeding disorders, p468; Electrolyte management, p482; Infe ction control \200\224general principles, p544; Pyrexia \200\224causes, p602; Pain, p618. This page intentionally left blank 623 Chapter 35 Oncological critical care Pain and comfort 624 Effects of chemo- and radiotherapy 626 Neutropaenia and infection 628 Leukemia/lymphoma 630 624 CHAPTER 35 Oncological critical care Pain and comfort Patients with oncological disease may complain of pain or discomfort relat ed to the neoplasm itself or as a consequence or complication of the treatment. Approximate ly 90% of patients with advanced cancer experi- ence severe pain that is often under-treate d. Pain management may be further complicated by a chronic dependency on analgesia, necessi tating high doses for managing acutely painful episodes.