Viral haemorrhagic fever (VHF) VHF is a group of viral infections that cause a severe haemo rrhagic disease. They include Lassa, Ebola, and Marburg fevers. Treatment is supportive and mortality high for these highly contagious pathogens. In some countries, such patients are managed in a high-risk Infectious Diseases Unit with per- sonal protective equipment for s taff. These units generally have restricted access, lobbied entrance to isolation rooms, ne gative pressure with HEPA \201 ltration for exhaust air, en suite facilities, and staff s hower and change facilities. Protective suits limit the time staff can work to four hours. In other countries, these patients are managed in bed isolator tents (Trexler units) with t he provision of all care via invaginated sleeves into the tent. The provision of intensive care within a Trexler tent is nearly impossible. H5N1 H5N1 is an avian in \202 uenza A virus that has caused illness in humans. There is ev idence of limited human-to-human transmission and transmission of the virus to those handli ng of infected poultry. Around 60% of humans known to have been infected with the recent As ian strain have died. H5N1 may mutate into a strain capable of ef \201 cient human-to-huma n transmis- sion. Treatment is supportive although oseltamivir may inhibit the virus from s preading within the body. SARS, VHF, AND H5N1 571 See also: Infection control \200\224general principles, p544; Infection control \200\224dan gerous pathogens, p548. 572 CHAPTER 31 Infection and in \202 ammation Rheumatic disorders Rheumatoid arthritis A debilitating arthritis that may present to criti cal care through pulmo- nary involvement or through complications of treatment (e.g. renal failure, immunosuppression, bleeding disorders). Pleuro-pulmonary involvement may precede a rthritic symptoms and is more common in those with active rheumatoid disease and middle-age d men. Care is required when intu- bating patients with rheumatoid arthritis since the neck joints may sublux. Advice should be sought from a rheumatologist about starting/continuing treatment with steroids or other disease modi \201 ers such as methotrexate, anti-TNF ant ibody, or rituximab. Rheumatoid pleurisy Often presents with effusion and can be asymptomatic. Effusions may be recurrent or chronic and may impede respiratory function. The effusion is an exudate, low i n glucose, and often high in cholesterol. Rheumatoid lung A diffuse interstitial pneumonitis with bibasal \201 brotic changes on ch est X-ray or CT. It produces a restrictive pulmonary defect. The mainstay of treatment is e arly systemic corticosteroid therapy. Systemic lupus erythematosis (SLE) A non-organ speci \201 c autoimmune disease characteriz ed by anti-nuclear antibodies with high titres of anti-double stranded DNA antibodies. Vasc ulitis is prominent though cutaneous and CNS involvement are not vasculitic. SLE may presen t to intensive care through pulmonary, renal, or central nervous system involvement. Renal failure Renal failure is vasculitic in origin and may progress to end-stage renal fai lure requiring long-term dialysis. Early treatment with systemic steroids and immunosuppres sives may halt the disease progress. Lupus pleurisy and pericarditis Unlike rheumatoid pleurisy, pleural involvement in SLE is o ften painful and associated with large pleural effusions. Pulmonary hemorrhage This is associated with renal failure and may be life-threatening. Pla sma exchange may be helpful. Interstitial pneumonitis Interstitial pneumonitis is uncommon. Parenchymal in \201 ltrates are more likely to be infective in origin, secondary to immunosuppressive therapy. Pulmonary thromboembolic disease Patients typically have a prolonged APTT due to circulatin g lupus antico- agulant but are more prone to thrombotic episodes. Lupus anticoagulant is a ssociated with anticardiolipin antibodies. Recurrent pulmonary emboli may be associated wit h chronic pulmonary hypertension. Treatment is long-term anticoagulation. RHEUMATIC DISORDERS 573 See also: Respiratory imaging, p158; Anticoagulants, p318; Corticosteroids, p328; Rituximab , p334; Pulmonary embolus, p376; Acute renal failure \200\224diagnosis, p400; Acute renal f ailure \200\224management, p402; Vasculitis, p574. 574 CHAPTER 31 Infection and in \202 ammation Vasculitis Vasculitis should be suspected in any patient with multisystem disease, especial ly involving the lungs and kidneys. Wegener \200\231s granulomatosis A systemic vasculitis characterized by necrotising granulo mas of the upper and lower respiratory tract, glomerulonephritis, and small vessel vasculit is. Wegener \200\231s granulomatosis is associated with positive core anti-neutrophil cytop lasmic antibodies (c-ANCA), particularly granular with central attenuation on immuno \202 uorescence. Intensive care admission is usually because of renal and pulmonary involvement. Renal failure Focal necrotising glomerulonephritis leads to progressive failure. Treatment with steroids and cyclophosphamide may give complete remission. Upper airway disease Nasal symptoms include epistaxis, nasal discharge, and septal perforat ion. Critical care admission may be required for severe epistaxis. Ulcerating lesions of th e larynx and trachea may cause subglottic stenosis. This is usually insidious but may prese nt problems on attempted intubation. Pulmonary involvement Usually associated with haemoptysis, dyspnoea, and cough with rounded opacities 9 cavitation on chest X-ray/CT. Nodules may be solitary. Alveolar hemorrhage may be life-threatening. The mainstay of treatment is steroids and cyclophosphamide which may produce complete remis- sion. Plasma exchange may be helpful. Polyarteritis nodosa (PAN) PAN is a necrotising vasculitis affecting small and medium-sized mus- cular arteries. Intensive care admission may be provoked by renal failure, ischaemic heart disease, hypertensive crisis, and bronchospasm although true pulmonary involvement is uncommon. Diagnosis may be con \201 rmed by mesenteric angiography or renal biopsy. Treat ment involves renal replacement therapy, high dose steroids, and cyclophosphamide. Goodpasture \200\231s syndrome Anti-glomerular basement membrane (anti-GBM) antibodies bind at the glomerulus and alveolus. Patients present with a proliferative glomeru- lonephritis and haemoptysis. Diagnosis is con \201 rmed by positive anti-GBM antibodies and renal bio psy. Treatment is with immunosuppressive therapy and plasma exchange. VASCULITIS 575 See also: Plasma exchange, p114; Corticosteroids, p328; Airway obstruction, p348; Haemoptys is, p372; Acute renal failure \200\224diagnosis, p400; Acute renal failure \200\224manageme nt, p402; Rheumatic disorders, p572. 576 CHAPTER 31 Infection and in \202 ammation Toxic epidermal necrolysis Toxic epidermal necrolysis (TEN) is an acute onset, potentially life-threatening, idiosyncratic mucocutaneous reaction, usually occurring after starting a new drug, e.g. antibiotics, non-steroidal anti-in \202 ammatory drugs, anticon- vulsants, allopurinol or, less commonly, immunization. It is often compli- cated by infection and mul ti-organ dysfunction. Mortality is 25 \200\22375%, often from secondary sepsis. Clinical features \200 \200 There is often a \202 u-like prodrome for 2 \200\2233 days. Macular rash that may become con \202 uent, with desquamation of skin and mucosae leaving raw, moist, denuded surfaces. Conjunctivitis may precede skin changes by 1 \200\2233 days. More common in women patients with HIV disease. Relevant drugs will have been started within the previous four weeks. \200 \200 Management \200 Clinical diagnosis is usually suf \201 cient; skin biopsy may be needed for atypical cases . Stop all potential causative drugs. Intravenous catheters should avoid involved skin, if possible. A SCORTEN assessment should be made. Patients with SCORTEN \211 2 or signi \201 cant comorbidity should be managed in a critical care facility. Fluid loss from desquamati on mandates careful assessment and replacement of \202 uid. Requirements approach those n eeded for an equivalent burn injury. Give oral or intravenous analgesia. Give thromboprophy laxis. Regularly assess for infection and sepsis. Hypothermia may indicate the onset of sep sis. Since TEN patients are susceptible to infection, they should be managed in protective isolation Manage patients on a pressure-relieving mattress in a humidi \201 ed environment . Early attention to eye care is essential. Apply chloramphenicol eye ointment 6-hourly (un less chloramphenicol is a possible causative agent). Desquamation may obstruct the tracheob ronchial tree or urethra. Avoid adhesive tapes and do not debride skin. Detached skin shoul d be left in place and protected with 50:50 white soft paraf \201 n. \200 \200 \200 \200 \200 TOXIC EPIDERMAL NECROLYSIS 577 SCORTEN indicators of prognosis Age more than 40 Heart rate more than 120/min Malignancy >10% body surface area blistered at day 1 Urea >10mmol/L Bicarbonate <20mmol/L Glucose >14mmol/L Mortality up to 10% for 1 indicator, 10 \200\22319% for 2, 20 \200\22339% for 3, 10 \200 \22359% for 4, and >60% for >5. Key Paper Bastuji-Garin S, Fouchard N, Bertocchi M, et.al. (2000) SCORTEN: a severity-of-il lness score for toxic epidermal necrolysis. J Invest Dermatol 115: 149 \200\22353. See also: Wound and pressure sore management, p134; Wound management principles, p136; Dres sing techniques, p138; Special support surfaces, p140; Basic resuscitation, p338; Fluid cha llenge, p342; Infection \200\224diagnosis, p552; Infection \200\224treatment, p554; Pain, p 618. 578 CHAPTER 31 Infection and in \202 ammation Anaphylactoid reactions Minor reactions to allergens (itching, urticaria) are common before a severe reaction occurs; any such history should be taken seriously and potential allerge ns avoided. Most reactions are acute in onset and clearly related to the causative allergen . However, some complement-mediated reactions may take longer to develop. Clinical features \200 Respiratory \200\224laryngeal oedema, bronchospasm, pulmonary oedema, pulmonary hypertensio n. Cardiovascular \200\224hypotension, tachycardia, generalized oedema. Other \200\224urtic aria, angio-oedema, abdominal cramps, rigors. \200 Management 1. Stop all infusions and blood transfusions, and withhold any potential drug or food allergen. Blood and blood products should be returned to the laboratory for analysis. 2. Give appropriate oxygen to maintain normoxaemia. If hypoxaemia per- sists, consider urgent intubation and mechanical ventilation. 3. If there is laryngeal obstruction, bronchospasm, or facial oedema, give IM or nebulised adrenaline and IV hydrocortisone. If there is no rapid relief of airway obstruction, consid er urgent intubation or, in extremis, emergency cricothyroidotomy or tracheostomy. Persiste nt bronchos- pasm may require epinephrine 9 salbutamol 9 aminophylline infusion, or assiste d expiration (manual chest compression). 4. Treat hypotension with adrenaline IV/IM and rapid colloid infusion. Large volumes of col loid may be required to replace the plasma volume de \201 cit in severe anaphylaxis. \200 \200 Severe oedema may coexist with hypovolaemia. Plasma volume has not been adequately replaced if the hemoglobin is higher than normal. 5. Treat persistent hypotension with further epinephrine, hydrocortisone, and colloid infus ion guided by CVP 9 cardiac output monitoring. Use norepinephrine in high output vasodilato ry shock to divert blood cen- trally and increase peripheral resistance. 6. Urticaria requires chlorphenamine IV or PO, depending on the severity of the reaction. 7. After control of the anaphylactoid reaction, advice should be sought from the immunology laboratory and appropriate samples taken for con \201 rmation. 8. Reactions to long-acting drugs or \202 uids will require continued support (perhaps for many hours). ANAPHYLACTOID REACTIONS 579 Drug dosages Initial dose Continued treatment Laryngeal oedema and bronchospasm Epinephrine 0.3 \200\2230.5mg IM or 0.5mg nebulised Start at 0.05mcg/kg/min Hydrocortisone 200mg IV Hypotension Epinephrine 0.5 \200\2231.0mg IM or 0.05 \200\2230.2mg IV Start at 0.05mcg/kg/min Colloid 500mL According to response Hydrocortisone 200mg IV 200mg IV qds Chlorphenamine 10mg IV tds Urticaria Chlorphenamine 10mg IV tds or 4mg PO tds Hydrocortisone 50 \200\223100mg IV tds Prednisolone 20mg PO daily See also: Endotracheal intubation, p42; Bronchodilators, p254; Inotropes, p264; Corticoster oids, p328; Basic resuscitation, p338. This page intentionally left blank 581 Chapter 32 Trauma and burns Multiple trauma (1) 582 Multiple trauma (2) 584 Head injury (1) 586 Head injury (2) 588 Spi nal cord injury 590 Burns \200\224 \202 uid management 592 Burns \200\224general managemen t 594 Blast injury 596 582 CHAPTER 32 Trauma and burns Multiple trauma (1) Such patients are admitted either after surgery or for close observatio n and medical management. The principles of management are to: \200 \200 \200 \200 \200 Maintain or quickly restore adequate tissue perfusion and gas exchange. Control pain. Secur e haemostasis and correct any coagulopathy. Provide adequate nutrition. Monitor closely and deal promptly with any complications. Circulatory management \200 Patients are often cold and vasoconstricted on admission. This can camou \202 age concurre nt hypovolaemia and compromise perfusion. Institute adequate monitoring at an early stage. Development of a persisting tissue oxygen debt has been shown to lead to subsequent multipl e organ dysfunction which may not become clinically apparent for 3 \200\2237 days. Therefor e, adequate perfusion must be restored promptly by repeated \202 uid challenges. Addition of a vasodilating agent, e.g. glyceryl trinitrate, may be bene \201 cial. An early increa sing metabolic acidosis should prompt suspicion of inadequate resuscitation, covert hemorrh age, or tissue necrosis. Myocardial depression or failure may also be implicated. \200 Respiratory management \200 If ventilated, ensure haemodynamic stability, removal of any metabolic acidosis, adequate r ewarming, and satisfactory gas exchange before attempting to wean. If the patient remains u nstable, it is advisable to delay extubation in case urgent surgery is required. If spontan eously breathing, give supplemental oxygen to provide adequate arterial oxygenation, encour age deep breathing to prevent atelectasis and secondary infection, and ensure suf \201 cie nt analgesia albeit not too much to suppress ventilatory drive. Hematological management \200 Initially maintain hemoglobin >9 \200\22310g/dL to assist oxygen transportation and provide a buffer for any sudden onset new hemorrhage. Crossmatched blood should be readily availab le. Correct coagulopathy as appropriate with fresh frozen plasma 9 platelets, and, occasion ally, other blood products (e.g. cryoprecipitate) or activated factor VII. Seek advice from a hematologist. Surgery or arterial embolisation may be needed for ongoing blood loss. Peripheries Injury to the limb may result in nerve injuries, obstruction of the vascular su pply, or muscle damage which may lead to compartment syndrome and rhabdomyolysis. A high le vel of suspicion should be held and corrective surgery undertaken promptly if necessary. En sure plaster casts do not compromise peripheral limb perfusion. MULTIPLE TRAUMA (1) 583 See also: Trauma score, p34; Ventilatory support \200\224indications, p44; Wound management principles, p136; Dressing techniques, p138; Blood transfusion, p248; Blood products, p250 ; Multiple trauma (2), p584; Head injury (1), p586; Head injury (2), p588; Spinal cord inju ry, p590; Coagulants and anti \201 brinolytics, p322; Basic resuscitation, p338. 584 CHAPTER 32 Trauma and burns Multiple trauma (2) Analgesia \200 Adequate analgesia is imperative to avoid circulatory instability and decreased chest wall excursion, especially following chest, abdominal, or spinal trauma. Increased use of region al techniques (depending on absence of infection and coagulopathy) and patient-controlled a nalgesia have facilitated pain relief and weaning. Opiates are recommended for initial anal gesia. Non-steroidals are particularly effective for bony pain though may occasionally prec ipitate coagulopathies, stress ulceration, and renal failure. Agitation may be due to cause s other than pain, e.g. infection, intracranial lesion, alcohol, or recreational drug withd rawal. Nutrition Early nutrition has been shown to reduce post-operative complications. This shoul d ideally be enteral, an approach which has been demonstrated as safe even after abdominal laparotomy for trauma. Infection \200 Depending on the site of trauma, the type of wound (open/closed, clean/dirty), and the need for surgery, prophylactic tetanus, and antibiotic cover varying from 1 dose to 1 \200\2232 weeks may be needed. The trauma patient is at high risk of developing secondary infection, in particular, chest, wound sites, intravascular catheter insertion sites and, post-abdomi nal trauma, intra-abdominal abscesses. Preventive measures and strict infection control sho uld be undertaken. Replace intravascular catheters inserted during emergency resuscitation under non-sterile conditions. Prophylaxis \200 Attention should be paid to pressure areas; this may involve the use of specialized mattres ses or support beds. Clear instructions should be obtained from the surgeon regarding care of the wound and drain sites. Deep venous thrombosis is common after trauma, especially aft er orthopedic procedures on the pelvis and lower limb. Discuss with the surgeon when to com mence low molecular weight heparin in view of any ongoing bleeding risk. Review \200 Regular review of the patient is necessary to ensure complications are detected and dealed with promptly. This may require repeat laparotomy, angiography, ultrasound, or CT/MRI scann ing. Later complications include pancreatitis, acalculous cholecystitis, and multiple organ dysfunction (including ARDS). MULTIPLE TRAUMA (2) 585 See also: Nutrition \200\224use and indications, p126; Wound management principles, p136; D ressing techniques, p138; Special support surfaces, p140; Non-opioid analgesics, p302; Opio id analgesics, p304; Anticoagulants, p318; Infection control \200\224general principles, p5 44; Infection \200\224diagnosis, p552; Infection \200\224treatment, p554; Systemic in \202 ammation/multi-organ failure \200\224causes, p556; Multiple trauma (1), p582; Pain, p618. 586 CHAPTER 32 Trauma and burns Head injury (1) The head may be injured with or without signi \201 cant trauma to other pa rts of the body. Priority in management of the multiply injured patient must be placed on s ecuring adequate gas exchange and circulatory resuscitation, and dealing with any life-thre atening injury, e.g. an arterial injury, before de \201 nitive treatment for head injury. The patient will usually be admitted to critical care after CT scanning has identi \201 ed the extent of injury. The neck should also be imaged by CT, particularly if the patient is ventilated. It is also likely that surgery will already have been undertaken for any signi \201 cant space-occupying lesion or for elevation of a depressed fracture. General management \200 \200 See http://www.nice.org.uk/Guidance/CG56/Guidance/pdf/English. Assume an unstable neck frac ture until excluded by an expert opinion and appropriate investigations. Most head injury p atients admitted to non-neurosurgical Critical Care Units will have diffuse or local brain injury for which a non-operative approach has been adopted. The regional Neurosurgery cente r should be contacted if raised intracranial pressure is present as local policy may encour age early bone \202 ap decompression or referral for invasive monitoring (e.g. intracrani al pressure, jugular venous bulb O2 saturation). If a basal skull fracture is suspected (e. g. X-rays, rhinorrhoea, otorrhoea), avoid nasal insertion of feeding or endotracheal tubes. Deterioration in conscious level, developing neurological de \201 cits or focal signs (e. g. unilateral pupillary dilatation) should prompt urgent repeat CT scanning for late compli cations, e.g. subdural haematoma. Complications \200 \200 Actively manage raised intracranial pressure. Actively treat seizures with anticonvulsants to prevent further hypoxaemic cerebral damage, reduce cerebral oxygen requirements, and ICP . Load with IV phenytoin as prophylaxis against further \201 ts. Consider additional caus es such as hypoglycaemia, development of a new space-occupying lesion, recreational drugs ( or withdrawal), and infection. Diabetes insipidus suggests hypothalamic injury and carries a poor prognosis. Desmopressin 1 \200\2234mcg IV should be given daily to maintain urine ou tputs of 100 \200\223150mL/h. Actively manage hyperpyrexia. Some studies show long-term ben e \201 t from induced hypothermia; this needs to be aggressively instituted as early as po ssible after the injury to be most effective. Ensure good glycaemic control with insulin as needed. Avoid hypoglycaemia. HEAD INJURY (1) 587 Key papers Rovlias A, Kotsou S. (2000) The in \202 uence of hyperglycemia on neurological outcome in patients with severe head injury. Neurosurgery 46: 335 \200\22342. Clifton GL, Miller ER, Choi SC et al. (2001) Lack of effect of induction of hypothermia aft er acute brain injury. N Engl J Med 344: 556 \200\22363. See also: Therapeutic hypothermia, p100; Tight glycaemic control/intensive insulin therapy, p132; Intracranial pressure monitoring, p200; Jugular venous bulb saturation, p202; Other neurological monitoring, p206; Anticonvulsants, p312; Neuroprotective agents, p314; Basic r esuscitation, p338; Generalized seizures, p444; Intracranial hemorrhage, p448; Raised intra cranial pressure, p454; Multiple trauma (1), p582; Multiple trauma (2), p584; Head injury ( 2), p588; Spinal cord injury, p590; Pyrexia \200\224 causes, p602; Pyrexia \200\224manageme nt, p604; Hyperthermia, p606. 588 CHAPTER 32 Trauma and burns Head injury (2) Analgesia \200 Adequate analgesia (usually opiates) must be given to the head-injured patient as pain and agitation will increase intracranial pressure, thereby causing a secondary insult. Short-ac ting sedation should be used as this enables rapid assessment of the underlying conscious l evel and any focal neurological de \201 cit. Respiratory management \200 Aggressive hyperventilation is no longer recommended apart from short-term management of ra ised intracranial pressure. If ventilated, aim to maintain PaCO2 at 3.5 \200\2234kPa. Face or neck injuries may have required emergency cricothyroidotomy or tracheostomy to obtain a patent airway. If orotracheally intubated, ensure local swelling has subsided (nasendoscopy , air leak around de \202 ated cuff) before extubation. Severe agitation and confusion may last for several weeks; this will often delay weaning and extubation. Judicious sedation, e.g. with haloperidol, may be necessary. Circulatory management \200 \200 \200 Avoid hypotension with adequate \202 uid resuscitation 9 vasopressor. Elevated blood pres sures may be tolerated unless excessive. B-blockers are useful in reducing the myocardial a nd immunosuppressive effects of excessive catecholamine levels. Other drug therapy \200 \200 \200 Antibiotic prophylaxis is not routinely recommended. High-dose steroid therapy has not been shown to be bene \201 cial. Trials of other neuroprotective agents, e.g. free radical sca vengers, have also failed to show bene \201 t. Indications for consideration of intracranial pressure monitoring Indications \200 \200 Glasgow coma score \211 8 and any abnormality on CT scan. GCS \211 8 and a normal CT scan , but any two of the following: (i) age >40y, (ii) hypotension, (iii) decerebrate posturing . GCS >8, but requiring general anesthesia for treatment of other injuries or requiring tre atment likely to increase ICP, e.g. high levels of PEEP. ICP monitoring should be continued as long as the ICP is elevated, during active management of ICP, or for up to 3 days in the absence of signi \201 cant elevation. Contraindications \200 Coagulopathy. \200 Infection. HEAD INJURY (2) 589 See also: Ventilatory support \200\224indications, p44; Tracheotomy, p80; Intracranial pres sure monitoring, p200; Non-opioid analgesics, p302; Opioid analgesics, p304; Sedatives and tranquilisers, p308; Head injury (1), p586; Pain, p612. 590 CHAPTER 32 Trauma and burns Spinal cord injury Spinal injury, with or without damage to the cord, may be apparent soon after admission to hospital. However, deterioration may occur, requiring a high index of su spicion and careful monitoring. Immobilization \200 Immobilize the spine until a senior surgical/orthopedic opinion has con \201 rmed that no unstable fracture is present. Place a hard cervical collar and immobilize head with lateral supports. This does not stabilize the spine; either skull traction or operative stabilizat ion will be needed for an unstable fracture. Move the patient by \200\230log-rolling \200 \231 or straight-lifting, using at least four staff members. Exercise care with neck manipu lation; intubation should be performed by an experienced operator. Circulatory instability \200 So-called \200\230spinal shock \200\231 may occur with marked hypotension due to sympathet ic out \202 ow disturbance. Hypovolaemia should be excluded \201 rst. Consider damage to other organs/vessels, e.g. spleen, aorta. Vasopressor therapy may be necessary if evidence of tissue hypoperfusion persists, e.g. oliguria, metabolic acidosis. Postural hypotension and circulatory instability (including symptomatic bradycardia) is commonplace for the \201 rst few weeks. Autonomic dysfunction affects 50% of cervical and high thoracic cord in juries. Respiratory management \200 High cervical cord injury above C5 results in loss of diaphragmatic function. Injury above C8 can result in loss of intercostal function. This may compromise or prevent breathing and weaning from IPPV. When able, the patient should be managed in an upright posture. Atelect asis is common and requires regular physiotherapy. Early tracheostomy may facilitate suppor t and comfort. \200 \200 General measures \200 Carefully monitor neurological function to enable early detection of spinal cord compressio n and referral for urgent remedial surgery. Give LMW heparin SC for thromboembolism prophyl axis. The incidence of stress ulceration is high. Use enteral nutrition at an early stage. Drugs (e.g. H2-blockers) may be needed. Enteral feeding may be dif \201 cult to institute initially as gastric distension and paralytic ileus are common. An NG tube should be insert ed for gastric decompression. An enterostomy may be needed for feeding. Bowel and bladder f unction may be deranged. Insert a silastic bladder catheter. Regular laxative and enema the rapy should be started early. Special care is needed to prevent pressure sores. Institute r egular exercises to prevent contractures. Psychological support for patient and family is c rucial, particularly if long-term disability is likely. High-dose steroid therapy may be be ne \201 cial if started within 8h, though this still remains controversial. Hyperbaric oxy gen therapy is of unproven bene \201 t. After spinal injury, muscle relaxants may cause se vere hyperkalaemia. \200 \200 \200 \200 SPINAL CORD INJURY 591 Key papers Bracken MB, Shepard MJ, Holford TR, et al. (1997) Administration of methylpredni solone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spin al cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlle d Trial. National Acute Spinal Cord Injury Study. JAMA 277: 1597 \200\223604. Morris CG, McCoy W, Lavery GG. (2004) Spinal immobilization for unconscious patients with m ultiple injuries. BMJ 329: 495 \200\2239. See also: Ventilatory support \200\224indications, p44; Tracheotomy, p80; Chest physiothera py, p90; Enteral feeding and drainage tubes, p122; Wound and pressure sore management, p136 ; Special support surfaces, p140; Vasopressors, p268; H2 blockers and proton pump inhibitor s, p286; Anticoagulants, p318; Corticosteroids, p328; Multiple trauma (1), p582; Multiple t rauma (2), p584. 592 CHAPTER 32 Trauma and burns Burns \200\224 \202 uid management Major thermal injuries (i.e. >20% body surface area) ar e admitted to an Intensive Care Unit, usually specialized in the management of burns, for m eticulous attention to \202 uid resuscitation, prevention of infection, and the frequent need for mechanical ventilation. Monitoring \200 Fluid loss from major burns requires careful assessment of intravascular volume status. Tra ditional markers of \202 uid resuscitation such as CVP, urine output, and haematocrit are often inadequate. Either invasive or non-invasive cardiac output monitoring is needed for accurate titration of \202 uid. This is particularly applicable in the presence of a hype rdynamic, vasodilated circulation which often commences within 1 \200\2232 days. Although i nfection is not necessarily present, vasopressors may be needed to maintain an adequate sys temic BP. Intravascular catheters should not be inserted through affected skin areas, if at all possible. Insertion of intravascular catheters, urinary catheters, and NG tubes should be carried out soon after admission as rapid onset swelling within a few hours may make th ese procedures impossible. Fluid management \200 The extent of injury will have been estimated by plastic surgeons who will also determine t he proportion of full thickness dermal injury to calculate the approximate \202 uid resus citation required. Fluid resuscitation in the UK often follows the Mount Vernon (albumin- b ased) formula while the Parkland (crystalloid-based) formula is often used in the US. Collo ids may reduce oedema at non-burn sites and restore blood volume faster than crystalloids. These formulas only provide an approximate guide and frequently underestimate losses both i nto the interstitial spaces and through the lost skin barrier. Evaporative losses are appro ximately 2mL/kg/h. Water losses may be increased if wounds are not covered. Losses increase further with inhalation injury. Overzealous \202 uid infusion should be avoided to minim ize oedema. The increased permeability and \202 uid leak phase lasts approximately 1 \200 \2232 days. After 2 \200\2235 days, a diuretic phase usually commences when excess tissue \202 uid is lost and the body swelling reduces. Electrolyte levels (especially K+ and Mg2+ ) can \202 uctuate widely in both periods, requiring monitoring and replacement as necess ary. Though some haemolysis may occur, blood transfusion requirements are usually low, but debridement will result in major blood loss often requiring major transfusion (>8 \200\2231 0U). A coagulopathy will often occur, in part due to a dilutional effect of the albumin inf usion. \200 BURNS \200\224FLUID MANAGEMENT 593 Fluid resuscitation regimens These regimens should be used as a guide only. In the Critical Care Unit, haemodynamic monitoring gives a better guide to \202 uid requirements. Adapted from Parkland formula \200 Total volume of Ringer \200\231s lactate for the \201 rst 24h = 4mL Ringer \200\231s lact ate solution x bodyweight [kg] x % burn. Half the volume is administered in the \201 rst 8h, the rest is delivered over the next 16h. 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 