Primary survey Patients in shock require simultanous \202 uid resuscitation and rapid ide nti \201 cation of possible causes. Clinical signs of a pelvic fracture include obvious de formity, and shortening or rotation of the leg. Bruising of the external genitalia and loin s, although speci \201 c, can be delayed. In the absence of obvious signs of fracture, pel vic instability may be detected by applying anterior \200\223posterior pressure, springing the iliac crests and pulling on the leg to detect axial instability. These maneuvers risk e xacerbating the bleeding, and should be performed only once, if at all. An AP X-ray of the pelvis (and chest) is an essential adjunct to the primary survey. Separation of the symphys is pubis by >1cm implies serious disruption. A rectal examination is essential to assess bl eeding, perfo- ration by bony fragments, a palpable pelvic haematoma or fracture, and anal tone. Urethral injury is much nore common in men, but may occur in women. Signs include: \200 \200 \200 Angiographic embolization If a laparotomy is not indicated, but evidence of bleeding contin ues, pelvic angiography with a view to embolization can be considered. However, shock due t o arterial bleed- ing accounts for only 10 \200\22320% of cases, and the type of frac- ture does not help predict the presence of arterial injury. One approach is to perform angiogra phy in patients after external fixation, who can be stabilized, but continue to require blo od transfusion at a rate of 1 \200\2232 units/h. Perineal bruising and scrotal haematoma Blood at the external urethral meatus High riding p rostate 491 CHAPTER 28.5 Pelvic trauma reduces hospital stay and long-term disability. However, the surgery can be challenging and lengthy, and should only be undertaken in stable patients. These patients can be safely transported to the angiography suite. The arteries most common ly damaged are branches of the internal iliac, the pudendal (anterior injuries) and the sup erior gluteal (damage to the sciatic notch). Angiographic embolization is unlikely to be pr actical in patients who are in extremis, losing up to 8 units/h. In these patients, pelvic packing at laparotomy can be considered. Complications Sepsis Haematoma resulting from pelvic fractures may become infected and form abscesses. Other local sources of infec- tion include \201 xation devices and wounds. If undiagnosed, extraperitoneal rupture of the rectum may form a pelvic abscess and systemic sepsis. Pelvic packing Laparotomy has traditionally not been indicated for a frac- tured pelvis alo ne, and hypogastric artery ligation is known to be ineffective. More recently a combination of external \201 xation, or C-clamps, with presacral and paravesical pack- ing has been employed in patients in severe shock, in whom the mortality is very high. Temporary aortic clamping can allow visualization and access. The rationale is that of \200\230dam- age con trol surgery \200\231; performing rapid life-saving interven- tions without attempting de \201 nitive treatment. Thromboembolism Thromboembolism is a major risk following trauma, and particularly followin g pelvic fractures, due to immobility, and damage to blood vessels. Prophylaxis should be g iven depending on other injuries, according to local protocols. Doppler ultrasound will det ect thrombi in the leg, but will not detect pelvic thrombi, which are more clinically signi \201 cant. Secondary survey The secondary survey is undertaken once life-threatening injuries have bee n stabilized. The purpose is to identify all other injuries. The urethra, bladder, rectum a nd neurovas- cular structures may all be damaged by pelvic fractures due to deformity, tear ing or penetration by bony fragments. In stable patients, a CT scan is the investigation of choice for de \201 ning the extent of these injuries. Pain Chronic pain syndromes may follow pelvic fractures, often due to damage to the sacroil iac joint, or leg-length discrepancies. Prognosis Mortality is primarily determined by the severity of the associated injuries, rat her than the pelvic fracture per se. Mortality is low (3 \200\2234%) in the absence of shoc k. Mortality is increased in the presence of a head injury, shock on pres- entation and inc reasing transfusion requirements. Those presenting in shock have a mortality of 50%. Poster ior pel- vic fractures have higher transfusion requirements and a higher mortality. Bladder, urethral and rectal injuries Extraperitoneal bladder rupture (80%) is more common than intraperitoneal rupture (20%), and in the majority of cases resolves with drainage and irrigation. Intraperitoneal bladder rupture requires emergency laparotomy. One- \201 fth of patients with bladder lesions have urethral injuries. These are managed initially by sup rapubic drainage, but complete tears will require subsequent urethroplasty. Impotence is as sociated with urethral injuries. Rectal per- foration is associated with bladder and urethr al injuries, and is most commonly extraperitoneal. A defunctioning colostomy may be require d. Further reading Advanced Trauma Life Support for Doctors, ATLS, faculty course manual. Chicago: American College of Surgeons, 2004. Gansslen A, Giannoudis P, Pape H-C. Hemorrhage in pelvic fracture; who needs angiography? C urr Opin Crit Care 2003; 9: 515-23. Nerve injuries The sacral plexus or sacral nerve roots can be damaged by fractures of the s acrum or sacroiliac joints. This results in loss of anal tone and perineal anesthesia. The sciatic nerve can be injured by fractures of the posterior acetabulum or greater sciatic no tch. The L5 root may also be damaged with sacral fractures. Injuries to the obdurator nerve are easily overlooked. Incaglioni P, Viggiano M, Carli P. Priorities in th management of severe pelvic trauma. Curr Opin Crit Care 2000; 6: 401 \200\2237. Shepherd C. eMedicine. Pelvic fractures. http://www.emedi- cine.com/emerg/topic203.htm. Thornton DD. eMedicine. Pelvic ring fractures. http://www. emedicine.com/radio/topic546.htm. Wheeles \200\231s textbook of orthopedics.; pelvic fractures menu. http://www.wheelessonline.com/ortho/pelvic_ fractures. De \201 nitive care Early internal \201 xation of unstable pelvic ring fractures with pl ates and screws allows more rapid mobilization, and 492 P FERRIS, R DUNCAN, & P NIGHTINGALE Burns \200\224 \202 uid management Introduction In the decades from 1930 to 1950 hypovolaemic shock and shock-induced renal fa ilure were the leading causes of death following signi \201 cant burn injury. It was then discov- ered that mortality could be improved by \202 uid resuscita- tion to replace the considerable post-burn intravascular \202 uid de \201 cits. Since then, numerous \202 uid resuscitation strat- egies have been developed. a lower risk of infection than the femoral veins, but choice is generally dictated by the d istribution of the burn. Full aseptic precautions are essential, and meticulous care of any central venous cannula is necessary to prevent infec- tion. Ultrasound guidance is recomme nded because even at an early stage, constricting burns and oedema can dis- tort the anatom y. Urine output is an important indicator of adequate res- uscitation, so all patients with burns of >20% or so TBSA should have a urinary catheter inserted early, as oedema formatio n can make insertion dif \201 cult later on. Oedema formation can be extensive and progres sive, so care must be taken when using any circumferential dress- ings (e.g. to secure IV a ccess) to avoid any tourniquet effect. Progressive oedema formation can also kink or dislod ge peripheral and central cannulae from the vein, so a high index of suspicion and regular assessments are necessary. Pathophysiology A burn injury results in an intense in \202 ammatory reaction involving nu merous in \202 ammatory mediators including his- tamine and bradykinin. This is exacerbate d by considerable endothelial oxidant damage (mainly of neutrophil origin), leading to incr eased capillary permeability that is exacer- bated by localized (or systemic) hypoxia. Inte rstitial oncotic pressure is increased by macromolecular fragmentation (caused by direct th ermal injury), and interstitial hydro- static pressure plummets to negative values due to t he sudden increase in osmotically active particles. These fac- tors promote the rapid shift of \202 uid into the interstitial space. Oedema formation is most rapid in partial thick ness burns, whereas in deeper injuries the oedema formation is slower, but of a greater mag nitude. In burns >25 \200\22330% of total body surface area (TBSA), these effects cease to be con \201 ned solely to burned tissues, and oedema formation becomes systemic. Leaking c apillaries can allow molecules of up to 300kDa (cf. red blood cells which are 350kDa. Album in (69kDa) escapes from the intravascular compartment, and experi- ments have shown that th e entirety of the body \200\231s serum proteins can be lost from the circulation within 24h of a 20% TBSA burn. The increased systemic capillary permea- bility usually resolves betwe en 8 and 24h post-burn, and is re \202 ected by a reduction in \202 uid requirements. Ja ckson classically, conceptualized three zones within a burn wound. \200 Fluid nanagement Post-burn \202 uid requirements are highly variable because of factors r elating to the patient, the presence of other inju- ries and those related to treatment, e. g. \202 uid requirements are increased by delayed resuscitation, inhalational injury and deeper burns. Predicting \202 uid requirements is not an exact science as in the last 60y rs or so numerous formulas have been derived to help in the estimation process. The main va riables dictating volume requirements are TBSA burnt, patient age and weight, and their int ubation status. None of the available formulas has been shown to be unquestionably superior , but the Parkland formula has been most commonly adopted worldwide. The Parkland formula a dvocates a total of 4ml/kg/% TBSA burn of lactated Ringer \200\231s solution (similar in co mposition to Hartmann \200\231s solution) in the \201 rst 24h post-burn (half to be given in the \201 rst 8h post-burn, and half in the next 16h). It must be emphasized that all formulas only act as a rough guide. A patient \200\231s requirements will not always be acc urately re \202 ected by such formulas, and they present at various time points following burn injury and in various states of hypovolaemia. It is therefore essential to be guided b y the clinical picture, as there are serious consequences to either over- or under-resuscit ation, and since widespread adop- tion of crystalloid burns resuscitation, the global trend has been to over-resuscitation. This iatrogenic injury is as dam- aging to morbidity and m ortality as under-resuscitation. By convention, IV \202 uid resuscitation is given to all adults with burns >15% TBSA, and all children ( \211 6 years) with burns >10% TBSA. Howeve r, due to poorer compensatory mechanisms (primarily within the renal and cardiovascular sys tems), elderly patients with burns <15% TBSA may also bene \201 t from parenteral resuscit ation. Recommendations regarding the \202 uid types to use have varied, but international ly, the most widely adopted stance is for crystalloids, at least initially, rather than col loid, for the following reasons: \200 Zone of coagulation (innermost) \200\224comprising irreversi- ble tissue loss Zone of ischa emia/stasis \200\224an area of damaged but potentially salvageable tissue which may progres s to necrosis if resuscitation is inadequate Zone of hyperaemia (outermost) \200\224tissues on the periphery of the burn that are minimally damaged, and will survive, but are hyperae mic in response to in \202 am- matory mediators As well as preventing circulatory collapse, proper \202 uid resuscitation can help salvag e potentially ischaemic tissues. Intravenous access Effective \202 uid resuscitation requires reliable IV access. In the \201 rst instance, two large bore cannulae will suf \201 ce, but major burns will often r equire central venous catheteriza- tion. Placing cannulae through burned skin is best avoid ed if possible, due to the heightened risk of infection and dif- \201 culty in siting and securing cannulae, but acceptable if there is no choice. Extensive burns may require a sur gical cut-down. If a central line is deemed necessary, it should be inserted early, as the inevitable oedema formation will make insertion much more dif \201 cult later. The interna l jugu- lar and subclavian veins are the preferred routes for central venous access, as the y give a more reliable CVP and carry Macromolecules up to 300kDa can leak from the circulation, negating the volume expansion b ene \201 t of colloids Colloids can accumulate in the interstitium, thus increas- ing loca l oncotic pressure and prolonging oedema Some colloids have been associated with signi \201 cant pruritis 493 CHAPTER 28.6 Burns \200\224 \202 uid management Many colloids have additional adverse effects, e.g. with starches, the larger the molecular size, the greater the coagulopathy. Monitoring acid \200\223base balance can be useful to reveal hypoperfusion-related acidosis , but interpretation may be compromised by exogenous organic or inorganic acids, poisoning by carbon monoxide and/or cyanide, ketoacidosis, poor renal function compromising clearance of acids, or even an occult compartment syndrome. The haematocrit (and other indicators of haemoconcen- tration) also contribute a minor role in monitoring, but interpretation is co mpromised by haemolysis, haemor- rhage, sequestration within burned tissues and rouleaux fo rmation. Cardiac output monitoring is not necessary for all patients, but is a useful adjun ct if there is reason to suspect many of the above conventional methods of monitoring are u nreliable or if the patient has either a huge burn injury or poor com- pensatory mechanisms , e.g. the elderly or those with heart disease. Monitoring trends is more useful than absol ute numbers as cardiovascular haemodynamics can be grossly deranged, and achieving \200 \230normal \200\231 physiological values may be either impossible or undesirable. When it i s thought that the patient requires more \202 uid, it is recommended to increase the rate of infusion rather than giving boluses (except in severe hypotensive episodes) because bol uses transiently cause high venous pres- sures which increase capillary leakage and hence o edema formation. When using crystalloid \202 uid resuscitation in major burns, abdominal compartment syndrome is a potential compli- cation. In large injuries, it is therefore advi sable to monitor intra-abdominal pressure (e.g. by transducing the urinary catheter). After the \201 rst 24h, \202 uid requirements reduce, but remain elevated above usual mainte nance volumes, and they are crudely predicted as 1ml/kg/% TBSA burn in 24h. By this stage, colloids are usually better retained within the circulation and can now be added if require d to enhance the intravascular colloid osmotic pressure and reduce the overall \202 uid v olume. For these reasons, colloids are generally avoided for the \201 rst 12 \200\22324h post-bu rn. However, crystalloids have their own disadvantages, primarily the considerably heighten ed volumes required, whose corollary is increased oedema formation and its consequences, e. g. higher incidence of compartment syndromes, including in unburned limbs. In the choice of crystalloid solution, iso- or hypertonic \202 u- ids are used, as they bene \201 t from the greatest volume expansion properties. Solutions mimicking plasma electro- lyte composi tion are favored, e.g. Hartmann \200\231s solution, as they more closely re \202 ect the c omposition of the lost \202 uid and, with their lower chloride concentration, present a l esser acid load compared with 0.9% sodium chloride. Monitoring Patients with major burns must be monitored closely and the \202 uid resuscita tion altered according to individual patient response. It is essential to use a variety of monitoring meth- ods to gauge overall response to \202 uid resuscitation, because numerou s factors complicate their interpretation. Urine output is probably the most useful paramet er to guide resuscitation, and should be maintained between 0.5 and 1.0ml/kg/h (1 \200\2231 .5 ml/kg/h in children <20kg). Note the recommendation of a target range, not merely a mini - mum target output. However, a physiological oliguria is to be expected after trauma and, also, haemochromogenuria and rhabdomyolysis are common in this patient population, which ma y compromise the utility of urine output as a monitoring tool. Treatment of the latter cond itions nor- mally involves maintaining a high urine output, but this necessitates over-resu scitation which may increase mor- bidity. We would, therefore, advise a low threshold for i nstituting haemo \201 ltration rather than excessive crystalloid administration. The pain and anxiety associated with burn injuries can cause heart rate and blood pressure to be mis leading con- sequent to high levels of endogenous catecholamines. Trying to correct fully a ny \200\230swing \200\231 in the arterial waveform by augmenting preload can also lead to overadministration of \202 uids. CVP may be misleading because of excessive catecho- lami nes, pulmonary vasoconstriction and elevated abdomi- nal compartment pressures. In major bu rns, the CVP has been found to correlate more closely with the latter than with intravascul ar \201 lling, so a high CVP is of little value, but a low value remains likely to indica te hypovolaemia; trends rather than isolated absolute values should guide therapy. Further reading Arturson G. Microvascular permeability to macromolecules in thermal injury. Acta Physiol Scand Suppl 1979; 463: 111 \200\2232. Baxter CR, Shires T. Physiological response to crystalloid resuscita- tion of severe burns. Ann NY Acad Sci 1968; 150: 874 \200\22394. Jackson D. The diagnosis of the depth of burning. Br J Plastic Surg 1953; 40: 588 \200\22396. Yowler CJ, Fratianne RB. Current status of burn resuscitation. Clin Plast Surg 2000; 27: 1 \200\22310. 494 P FERRIS, R DUNCAN, & P NIGHTINGALE Burns \200\224general management Epidemiology Burns are injuries caused by exposure to heat (moat com- mon) and electrical, chemical or radioactive agents. In the UK, 16 000 burns per year require hospitalization, of which 1000 are major burns requiring \202 uid resuscitation (half are children). The lower airways are instead more commonly injured by contamination with particulate matte r and chemical prod- ucts of combustion (usually acidic in nature). Early bron- choscopy sh ould be performed for diagnosis (document involved bronchi, mucosal injury (erythematous, p ale, dry or ulcerated) and particulate contamination (percentage of mucosal surface coated) . Endoscopic bronchial lavage (using 1.4% sodium bicarbonate solution) may help clear parti culate matter and neutralize acidic particles. This may need to be repeated and should be s upplemented with chest physiotherapy and 4 hourly nebulizers of 1.4% NaHCO3 until soot has cleared from sputum. Exclude carbon monoxide poisoning in all smoke inhala- tion injuries b y measurement of carboxy-Hb levels. Normally this is <1.0%, though those living in urban ar eas or who smoke may have levels >5%. Treatment is with 100% oxygen until the carboxy-Hb le vel is <2%. National guidelines All patients should be referred to the local Burns and Plastic Surgery Department (and, if being transferred, should arrive within 6h of injury). The regional Bur ns Center will either take over care or assess and advise regarding ongoing management. Som e offer a Burns Outreach Service to provide continuing support. If no spe- cialist burns be d is available locally, the National Burn Bed Bureau can locate the nearest suitable bed na tionally (Tel. 01384 215 576). History It is important to elicit an accurate history of events sur- rounding the injury: w hat happened, when and where? \200 Cardiovascular management Fluid requirements are highly variable as they depend upon many f actors, including patient weight, injury size and depth, inhalational injury and type of \202 uid administered. Recent trends have been to use the Parkland formula to guide likely crystalloid requirements, but such formulas are a guide only. Over-resuscitation is as harm ful as under- resuscitation, so consider de \201 ning upper as well as lower limits for ur ine output. Reliable IV access is essential, and can be placed through burns if options are limited. Did the injury occur indoors or outdoors? (inhalation injury) What was burning? (toxic fume s) Were they rescued or escaped independently? (implica- tions for duration of exposure) Wa s there an explosion? (blast injuries affecting lung, bowel, ears) Where were they found? ( consider occult injuries, e.g. if found in front of house, did they jump out an upper \202 oor window? ) Condition at scene? (unconscious or CPR at scene explains failure to reg ain consciousness after several days treatment due to hypoxic brain injury) \200 Burn size Burn size is quoted as a percentage of the TBSA, and should be assessed in hospit al using a Lund and Browder Chart (Appendix 2). Areas of epidermal depth burn (erythema onl y, no blistering) are excluded from the size estimation. With early assessments, burns may not yet have developed blisters, so such areas should be rubbed with gauze to see if this c auses epidermolysis. In burns are >25% TBSA, generalized oedema occurs. Assessment As for any major trauma, an ATLS-style assessment is indi- cated in the initial evaluation of patients with burns. Severity of injury is mainly dependent on: anatomical si te(s), burn size, burn depth, patient age and the presence of an inhalational injury. Burn depth Burn depth is de \201 ned anatomically (from super \201 cial to deep): epiderm al, super \201 cial dermal (SD), deep dermal (DD) and full thickness (FT). Burn depth can be assessed by the appearance and texture of the wound plus its vas- cularity and sensation . Deeper burns exhibit more pallor, \201 xed dermal staining, decreased vascularity (blan ching) and sensation. FT burns have a leathery texture from coagu- lated and contracted der mal macromolecules. The burn depth has implications for healing times, scar formation and r equirement for surgery \200\224signi \201 cant DD and FT burns require skin grafting. Burn s extending into the dermis have some non-viable tissue, which must be removed before re-ep ithelialization can occur (either natu- rally by autolytic enzymatic debridement, or surgic ally). Its persistence on the body exacerbates the in \202 ammatory response, releases tox ins and is an infection risk. Early surgery is therefore generally advocated. Respiratory management Burns to the head, neck or upper airways can cause consid- erable oe dema, leading to airway compromise and a dif \201 cult (or impossible) intubation. Any pat ient with burns to such areas should be seen by a senior anesthetist or intensivist to asse ss requirement for pre-emptive intubation. Signi \201 cant upper airway burns swell rapidl y and require prompt intubation. Delaying intubation may make it techni- cally dif \201 cu lt, so a watch and wait strategy should be avoided. One of the most sensitive symptoms is d evelop- ment of a hoarse voice. Intubation: if possible, in adults an ETT \211 8.0mm shoul d be used to allow diagnostic and therapeutic broncho- scopy without signi \201 cant venti latory compromise. The tube should not be cut to less that 28cm (still allows use of a gum elastic bougie) since major swelling causes it to retract intraorally. If marked swelling i s anticipated con- sider an armored tube or bite block (jaws may otherwise progressively cl amp the tube and occlude ventilation. The lower airways rarely sustain thermal injury due t o the effective heat exchange system in the upper airways. Escharotomies, fasciotomies and compartment syndromes Dermal contraction in greater than he mi-circumferential DD and FT burns can cause vascular (or respiratory) com- promise by a to urniquet effect upon limbs, neck or chest. 495 CHAPTER 28.7 Burns \200\224general management Positioning Head-up positioning can be used to reduce head and neck swelling, but a bed til t may be required rather than break- ing the bed, to minimize diaphragmatic splinting from intra- abdominal swelling. Long-term hand function can be improved using Bradford sling ele vation, regular physio- therapy and often splinting. Treatment is by escharotomy (incisions through burned skin to release constrictions). Swell ing limbs (even if unburned) can develop compart- ment syndromes, requiring fasciotomy (inc isions through deep fascia to release tight muscle compartments). Intra- abdominal hyperten sion (>12mm Hg) is common, and can progress to abdominal compartment syndrome requiring par acentesis, peritoneal drain or decompressive laparot- omy. Maintain a high index of suspici on; consider monitor- ing compartment pressures and the intravesical pressure. Myoglobinuria Extensive burns can result in haemoglobinuria from red cell destruction and, in deep burns involving muscle, rhab- domyolysis with myoglobinuria with the risk of acute renal failure. Measure serum creatine kinase and serum or uri- nary myoglobin soon after ad mission and, if elevated, main- tain a good urine output urinary alkalinization; haemo \201 ltration may be required. Dressings Patients being transferred to a local burns service usually have only cling- \201 lm applied to all non-facial burns (acts as a barrier to environmental contamination, reduces pain and evaporation and allows the burns team to visualize wounds). Beware of clin g- \201 lm rolling up and forming a tourniquet around the neck and limbs. The main cause o f mortality in burn injuries is infection, so treatment is focused upon maintenance of woun d cleanli- ness and regular microbiological surveillance; prophylactic antibiotics are not recommended. Dressings are used to allow the moist environment required for optimum wound h ealing whilst absorbing wound exudates, delivering anti- microbials to the wound surface, a voiding wound contami- nation and maintaining comfort. Burns should not generally be left e xposed. Prior to the \201 rst formal application of dressings, wounds should be cleaned ( soap and water will suf \201 ce), swabbed for organisms and blisters removed (not drained) to facili- tate burn assessment, remove necrotic tissue and allow contact of topical antim icrobials directly with wounds. Burn wounds should be photographed on admission for medicol egal documentation and to avoid repeated dress- ing removal for different clinicians to vis ualize the extent of the burn, thus reducing pain, contamination and heat loss. Many option s exist for dressings, but traditionally they comprise: a non-adherent layer (e.g. paraf \201 n tulle) with a topical antimicrobial applied (e.g. silver sulfadiazine or povidone-io dine), layers of absorbent woven gauze, then bandages. Dressings are changed daily or on al ternate days, or if exudates penetrate through outer bandages since their absorbency has be en lost and there is then an infec- tion risk. Grossly swollen hands and feet may be placed in a polythene bag containing antimicrobials to avoid restric- tive and constricting dress ings and permit easy visualization. Early management \200\224don \200\231t forget \200 Make an early accurate measurement of the patient \200\231s weight to guide \202 uid and nutritional requirements Consider potential self-harm, e.g. an overdose Insert an NG tube a nd start feeding within 6h of injury after adequate resuscitation Examine potentially injur ed eyes early, using \202 uorescein stain, before swelling prevents it Give tetanus toxoi d booster if required Ensure good analgesia Monitor core temperature and prevent or correct hypo- thermia: nurse in a cubicle at 30 C, warm all IV \202 uids, keep burns covered e xcept whilst assessing to reduce latent heat of evaporation (eventually a physiological pyr exia will develop) Beware coagulopathies from consumption of platelets and clotting factors , and from hypothermia Involve the whole multi-disciplinary team early including Physiother apist, Occupational Therapist, Dietician and Psychologist \200 \200 \200 Further information The one day internationally recognized Emergency Management of Severe B urns Course (EMSB) is held at various UK centers (see www.britishburnassociation. co.uk for details). Further reading National Burn Care Review Committee. Standards and Strategy for Burn Care, A review of burn care in the British Isles. 2001. This page intentionally left blank 497 Chapter 29 Physical disorders Chapter contents Hypothermia 498 Drowning and near-drowning 500 Rhabdomyolysis 502 Pressure sores 504 498 R VYAKNARAM & M JONAS Hypothermia De \201 ned as core temperature <35 C Mild 32 \200\22335 C; moderate 26 \200\22332 C; s evere <26 C cold \202 uid are aspirated into the lungs without immediate cardiac standstill. The ongo ing circulation results in rapid central cooling and potentially protection. More often, gl ottic spasm or onset of VF preclude this speed of cooling in nature, although it can be don e with an extracorporeal circulation. Risk factors Increasing age, abnormal mental state, immobility (ortho- paedic, Parkinsonism ), drugs (alcohol, barbiturate, major tranquilizers, antidepressants), endocrine (hypothyro idism, hyperglycaemia, adrenal insufficiency, hypopituitarism), autonomic neuropathy (diabe tes mellitus, Parkinsonism), malnutrition, renal failure, sepsis (excessive heat loss from vasodilatation), exposure (inadequate clothing/eating, near drowning). Complications VF, atrial tachy and bradyarrythmias, aspiration pneumonia, pancreatitis, bow el ischaemia, acute renal failure, rhab- domyolysis, DIC. Investigations \200 Presentation Mild hypothermia \200 Check core temperature using a low reading rectal ther- mometer Urgent bloods: U&Es, CK (de hydration, rhabdomyolysis), glucose (usually high), amylase (pancreatitis) Routine bloods: FBC, phosphate (d), magnesium (i), blood cultures, thyroid function test, toxic screen, ser um cortisol ABG: expect artefactual lower pH and higher PaO2 and PaCO2. Hence, to be correc ted to 37 C ECG: prolonged PR and QT intervals, J-waves <30 C (see Fig. 29.1.1) Urine: mi croscopy, culture and sensitivity (MCS), dipstick (blood and protein), myoglobinuria Shivering \200\224maximal at 35 C and decreases thereafter. Absent at <32 C. Mild confusi on, weakness, fatiguebility, lethargy, ataxia, dysarthia Progressive hypothermia \200 Delirium, coma, bradycardia and low respiratory rate, cardiac arrhythmias, dilated unrespon sive pupils and loss of re \202 exes EEG is \202 at at <20 C; asystole at <15 C Immediate hypothermia It has been suggested that very rapid hypothermia may occur in some c ases of drowning where large volumes of Treatment of severely hypothermic victims in cardiac arrest in the hospital setting should be directed at rapid J. Wave Fig. 29.1.1 In hypothermia, note the extensive J-waves; the patient is also in AF and has s igni \201 cant widespread T inversion. 499 CHAPTER 29.1 Hypothermia Cutaneous warming \200 core rewarming. Techniques that can be used include the administration of heated, humidi \201 ed oxygen (42 \200\22346 C (108.7 \200\223115 F), warmed IV \202 uids (normal sali ne) at 43 C (109 F) infused centrally at rates of 150 \200\223200ml/h (to avoid overhydr ation), peritoneal lavage with warmed (43 C (109 F)) potassium-free \202 uid administer ed 2l at a time, or extracorporeal blood warming with partial bypass. Pleural lavage with w arm saline instilled through a chest tube has also been used successfully. The routine admi nistration of steroids, barbiturates or antibiotics has not been documented to help increas e survival or decrease post- resuscitative damage. Passive insulation \200\224a single layer of any insulator (e.g. space blanket) reduces cut aneous heat loss by 30%. Active warming \200\224warm air via a air mattress/blanket. Activ e warming by resistive heating (electric) blankets is a recent development Internal warming \200\224 \202 uid warming to body temperature prior to infusion. The administration of 1l of fluid at room temperature decreases core temperature by 0.25 C. Airway humidi \201 ca tion \200\224this contributes little to preser- vation of core temperature because <10% of metabolic heat loss occurs via the respiratory tract. Prevention of hypothermia Heat loss occurs by radiation (60%), convection (25%), and evapor ation of body \202 uids (10%). General anesthesia typically results in mild core hypo- th ermia (1 \200\2233 C). As with general anesthesia, redistribu- tion of body heat during sp inal or epidural anesthesia is the main cause of hypothermia. There are three basic strateg ies for the prevention and treatment of mild hypothermia: 1 Minimizing redistribution of he at 2 Cutaneous warming during anesthesia 3 Internal warming. Invasive internal warming techniques \200 \200 Cardiopulmonary bypass Peritoneal dialysis Very effective but neither technique is relevant to mild hypothermia. Further reading Hayward JS, Eckerson JD, Kemna D. Thermal and cardiovascu- lar changes duri ng three methods of resuscitation from mild hypothermia. Resuscitation 1984; 11: 21 \200 \22333. Kirkbride DA, Buggy DJ. Thermoregulation and mild peri-operative hypothermia. Br J Anaesth CEPD Rev 2003; 3: 24 \200\2238. 500 G MORGAN Drowning and near-drowning Drowning is death from asphyxiation following submer- sion, usually in water. Incidents inv olving immersion or submersion may be referred to as \200\230near-drowning \200\231, a ter m which implies survival. Near-drowning is more common and many incidents are unreported. T hey tend to occur in childhood, early adulthood and in males, and are associ- ated with the use of recreational drugs, especially alcohol. Epilepsy, heart disease, CVA and deliberate self-harm are less common associations. (The practical distinction between immersion and s ubmersion may be unclear.) to a \202 oating object. At core temperatures of 33 \200\22335 C, muscle temperature may be as low as 28 C, precluding any purposeful movement. Consciousness Consciousness is impaired as temperature falls, until coma supervenes at 30 C. CBF is reduced and cerebral activity ceases at brain temperatures <22 C. In victims wh ose air- way is protected from aspiration of water by a life jacket or suspension in debris , cooling to temperatures <28 C may result in VF or a profound bradycardia and, at 24 \200 \22326 C, asystole. Children have a higher ratio of body surface area to mass, and cool fa ster than adults. It is likely that victims become hypothermic, lose consciousness and aspi rate water before cooling to a temperature suf \201 ciently low to provide cerebral protec tion. Under favorable circumstances, hypothermia may exert a positive in \202 uence on sur vival through a cerebral protective effect. However, this depends largely on the preservati on of cardiac output. In practical terms, when submersion in water occurs, initial voluntar y breath holding may be followed by components of the cold shock and diving responses. When breath hold- ing is overcome, involuntary gasping occurs and aspiration of water leads to laryngeal spasm. Vomiting may occur. Unconsciousness and death are inevitable without rescu e. Pathophysiological factors Aspiration of water into the lungs Aspiration of relatively smal l quantities of water alters sur- factant activity, causes atelectasis and produces hypoxia within a few minutes. People rescued conscious and alert may become hypoxic soon afterward s and take several days to recover normal levels of oxygenation. The effects of immersion in thermoneutral water With the head above water, hydrostatic pres sure to the chest and abdomen increases venous return and cardiac output by between 32 and 67%. Increased pulmonary blood volume, upward displacement of the diaphragm and compression of the chest wall combine to increase work of breathing by >60%. The effects of immersion in cold water (<25 C): cold shock and the diving re \202 ex With the head above water, the cold shock re \202 exes are triggered by a sudden fall in skin temperature. Increasing respiratory drive can generate a 10-fold increase in minute ventila tion in water at 10 C. Breath holding time is reduced to <10s. Peripheral vasoconstriction increases right atrial pressure and is accompanied by a tachycardia and an increase in car diac output of between 60 and 100%, which signi \201 cantly increases myocardial work. The se effects pre- vent effective breathing and swimming even in the young and \201 t, and a re suf \201 cient to cause MI or dysrrhythmia. The diving response, the purpose of which i s to conserve oxygen, is activated by immersion of the face in cold water. It is well devel oped in diving animals but is less predictable in humans, although more marked in infants. It is character- ized by apnoea, peripheral vasoconstriction and brady- cardia, and is medi ated via the ophthalmic division of the trigeminal nerve. In humans, the cold shock respons e is more marked than the diving re \202 ex. About 15% of humans have a marked diving re \202 ex which is accentuated in those wearing wet-suits or \200\230dry \200\231 immersion suits which leave only their face uninsulated against the cold environment. Rescue and subsequent management It is important to ensure the safety of personnel involved in rescue. Surface tension and G-force are suf \201 cient to cause circulatory collapse i n conscious victims lifted vertically, especially by helicopter. Rescuers should anticipate other illnesses and injuries, especially of the cervical spine. Management should proceed along standard ABC guide- lines with a view to transfer to an emergency department with acc ess to an intensive care facility. Categories of patient 1. Patients with no evidence of aspiration This group may have recove red substantially by the time they arrive at hospital, make light of the event and ask to b e discharged. They should be admitted and observed for 24h because of the risk of ALI and c erebral oedema. If they insist on leaving, they should receive instructions to return if th ey become unwell. 2. Patients with evidence of aspiration but without ventilatory compromise Pulmonary oedema may develop several hours after aspi- ration with rapid deterioration of ventilatory funct ion. Non-invasive or invasive ventilation may be required. Hypothermia and the value of a life jacket Hypothermia is a core body temperature of <35 C . The rate at which an immersed body cools depends on water temperature, movement of water over the skin, body surface area:mass ratio, insulation, peripheral circulation, metabolic rate and injuries or illness which may affect these. The summer time seawater temperature i n the UK is between 15 and 18 C.