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. 3. Patients with ventilatory compromise or hypothermia or both, but with a functional circu lation Hypothermic patients should be monitored in an ICU and actively warmed at 1 C/h. N IV may not be practical because of reduced level of consciousness, shivering or cardiovascu lar instability, in which case tracheal intubation and ventilation using a protective lung ventilation strategy should be started without delay. At 28 C there is a risk of ventricu lar arrhythmias. Neuromuscular function Peripheral cooling over 30min affects neuromuscular activity leadin g to \201 nger stiffness, poor coordination and loss of power, making it dif \201 cult t o initiate or maintain activities to assist survival, such as catching a rope or clinging 4. Patients in cardiac arrest \200\224the apparently dead CPR may be required for several h ours while the patient is warmed to 33 C by whatever means are available. 501 CHAPTER 29.2 Drowning and near-drowning monitoring is a priority for managing cardiac and circula- tory function. Initial assessment Renal Renal failure is common. Rhabdomyolysis may occur. ? Unconscious Yes Central nervous system Hyoxic brain injury may develop over 24 \200\22372h and may not be i mmediately evident on CT scan. ICP is a better guide to its development. ? Inadequate ventilation Intubate and Yes Hematological Aspiration of large quantities of fresh water into the circu- lation may caus e haemolysis. ? In cardiac arrest Yes Yes ? Aspiration No Re-warming \200 Victims who are conscious and not in ventilatory distress may be warmed in a bath at 40 C. Surface warming devices are also useful. In patients with no cardiac output, warming is mo st effectively achieved using cardiopulmonary bypass, from which there are encouraging resu lts. If this is not acces- sible, external cardiac massage must be continued while a variet y of techniques are employed to elevate the vic- tim \200\231s temperature to a level where spontaneous cardiac output returns or de \201 brillation is possible. None of these is ef \201 cient. Wet clothing should be removed, the skin dried, the vic- tim covered with war m blankets and kept out of drafts. A number of devices are available for application to a p atient \200\231s skin surface to control body temperature. Inspired ventilatory gasses shou ld be warmed to 45 C and humidi \201 ed. IV \202 uids should be warmed to 40 C and adm inistered through a warming device. Warmed water at 40 C may be instilled into the stom- a ch and bladder. Potassium-free peritoneal dialysis \202 uid at 40 C may be instilled int raperitoneally with a short dwell time. Once cardiac output has been restored, an intravasc ular warming circuit may be installed. Devices for regulating body temperature following ou t-of-hospital cardiac arrest and in the management of traumatic brain injury can be used to elevate a patient \200\231s temperature and may have a role in the subsequent control of b ody tempera- ture in this group of patients. A haemo \201 ltration circuit at a pump speed of 200ml/min can deliver 120kcal/h and also allows correction of acid \200\223base and ot her metabolic abnormalities. ALS and attempt rewarm to 33 C Admit to ICU Admit to ICU Admit to general ward for observation Fig. 29.2.1 Algorithm for the management of near-drowning. The diagnosis of death may present a problem while the patient remains hypothermic. General management Respiratory Hypothermia may cause rigidity unresponsive to neu- romuscul ar blocking agents. Circulatory compromise may render these drugs ineffective. Mouth openin g and tracheal intubation may be dif \201 cult. There is little practical differ- ence bet ween inhalation of fresh and salt water, but bacte- rial contamination may lead to unusual infections. Aspiration of gastric contents may occur at any time. Prophylactic antibiotics are usually omitted in favor of culture and active treatment of infection as it arises. ALI or ARDS may supervene. Radiographic abnormalities are common in patients without clinical evidence of aspiration. Acid \200\223base balance, blood gas analysis and metabolism Metabolic acidosis is common. Persistent lactic acidosis raises the possibility of hypoxic liver or bowel injury. Hyperka laemia is common during re-warming, re-perfusion and renal dysfunction. A potassium >10mmol /l with pro- found hypothermia is associated with asphyxial cardiac arrest and is not compa tible with successful resuscitation. Hyponatraemia may occur as a result of fresh water abs orption. Hyperglycaemia is common during initial resuscitation. Cardiovascular Hypothermia causes bradycardia with prolongation of the PR and QT interval, but a variety of supraventricular dys- rhythmias may occur. J-waves appear below 33 C. Bel ow 28 C the victim is likely to be in VF and requires re-warm- ing to >30 C so that de \201 brillation has a reasonable chance of success. De \201 brillation is hazardous to per sonnel in a wet environment. Troponin elevation may re \202 ect global myocardial hypoxaem ia and resuscitation rather than conventional MI. Pulse oximetry may be unreliable. It may be dif \201 cult to establish vascular access and the intraos- seous route should be consi dered early, even in adults. When spontaneous output has been established, invasive Prognostic indicators Survival Patients in categories 1 and 2 usually make good spontane- o us recovery, but serious organ system dysfunction may follow in patients in category 3. Pat ients in category 4 rarely survive. Outlook worsens in patients whose GCS is <9 or who have sustained a cardiac arrest which has not been rapidly recti \201 ed. Further reading Golden F StC, Tipton MJ, Scott RC, Immersion, near-drowning and drowning. Br J Anaesth 1997; 79: 214 \200\22325. 502 P STEVENS Rhabdomyolysis Electrolyte disturbance: hyperkalaemia, hypocalcaemia, hyerphosphataemia and hyperuricaemia . Creatinine levels are elevated out of proportion to urea levels and acidosis, and derange d liver function may also be apparent in 25% of patients. Rhabdomyolysis is disintegration of striated muscle. It is characterized by muscle necrosis leading to release of intracellular constituents into extracellular \202 uid and the cir culation. Causes include trauma, overexertion, substance abuse, muscle enzyme de \201 cien cies, electrolyte abnormalities, infections, drugs, toxins and endocrinopathies (Table 29.3 .1). Mechanisms of injury include direct injury to the cell mem- brane, muscle cell or hypo xia, leading to ATP depletion and sodium \200\223potassium pump failure. Extracellular calc ium ions leak into the cell and increase free cytosolic ionized cal- cium with activation o f calcium-dependent proteases and phospholipases, resulting in muscle destruction. Followin g muscle injury potassium, phosphate, myoglobin, creatine kinase (CK), creatinine and nucle osides (metabolized to urate) leak into the circulation. The muscle necrosis, in \202 am- mation and oedema lead to \202 uid accumulation in affected muscles and intravascular vol ume depletion. Early complications (within 12 \200\22324h) include hyperkalaemia, hypocalca emia and cardiac dysrhythmias, hepatic dysfunc- tion and early compartment syndrome. Late c omplications ( \211 24h) include acute renal failure, DIC, late compartment syndrome and (f ollowing recovery) hypercalcaemia. Prompt recognition and early intervention are therefore vital. Clinical manifestations Clinical manifestations are varied, dictated by the underly- ing cause and by the ensuing complications. Classic triad \200\224 muscle pain, weakness a nd passage of dark urine. Muscles may be tender and swollen. The most frequently involved m uscles are in the calves and lower back. Where pressure necrosis is part of the pathogenesi s, there may be overlying skin changes. In >50% of cases these \200\230local \200\231 mani festations may be absent. Urinary myoglobin concentration provides coloration ranging from pink-tinged through to muddy- brown/black. Systemic features include fever, malaise, nausea , vomiting, tachycardia, confusion and agitation. Oliguria/anuria may be apparent, and seve re hyperkalaemia may lead to cardiac dysrhythmia and arrest. Essential laboratory investigations \200 \200 \200 \200 \200 CK Urea, electrolytes and creatinine Calcium, phosphate and urate Blood gasses and urinary pH Clotting studies Table 29.3.1 Causes of rhabdomyolysis Trauma and compression Crush injury, road traf \201 c accident prolonged immobilization, e lectrical injury Ischaemic limb injury Exertional causes Marathon running, status epilepticus Heat-related causes Heat stroke, malignant hyperthermia and neuroleptic malignant syndrome Substance abuse Alcohol, cocaine, amphetamine, lysergic acid, Ecstasy Toxins Carbon monoxide, heavy metals, snake & insect venom Drugs Antipsychotics and antidepressants, sedative hypnotics, statins and \201 brates, th eophyllines Metabolic and endocrine causes Hypo- and hypernatraemia, hypocalcaemia, hypophosphataemia, hypocalcaemia, hypo- and hyperthyroidism, hyperosmolar conditions (HONK) Infectious causes Viruses: in \202 uenza and parain \202 uenza, coxsackie virus, adenovir us, echovirus, herpes viruses, CMV, HIV, EBV Bacteria: Streptococcus, Legionella, Salmonell a, Staphylococcus, Listeria, Tularaemia Other: Falciparum malaria, sepsis syndrome Laboratory features Laboratory \201 ndings con \201 rm the diagnosis and to an extent pr edict the prognosis in terms of complications. CK levels are the most sensitive indicator o f muscle damage and begin to rise within 12h of injury, peaking at 1 \200\2233 days and dec lining 3 \200\2235 days after injury. Supervention of compart- ment syndrome may lead to a secondary rise. The peak CK level is said to be predictive of acute renal failure, levels o f >16 000U/l being more likely to be associated with acute renal failure. Myoglobin has a m olecular weight of 18 800Da and in serum is bound to haptoglobin. Normal plasma levels of m yoglobin are very low (<30mcg/l). When >100g of skele- tal muscle are damaged, haptoglobin- binding sites are satu- rated and myoglobin is \201 ltered and appears in the urine. Norm al urinary levels of myoglobin are <5ng/ml, visible myoglobinuria (tea- or coca-cola-colore d urine) occurs when levels exceed 250mcg/ml. Myoglobin has a very short half-life (2 \200 \2233h) and serum levels return to normal within 6 \200\2238h. Therefore, although myoglobi n may be measured in both blood and urine, the clinical utility of such measure- ments is q uestionable. Genetic enzyme de \201 ciencies Myophosphorylase, phosphorylase kinase, phosphofructokinas e, phosphoglycerate mutase, lactate dehydrogenase, carnitine palmityl transferase, acyl-coe nzyme A dehydrogenase, mycoadenylate deaminase Autoimmune causes Polymyositis, dermatomyositis Complications of rhabdomyolysis Early complications Potassium, phosphate, creatinine, organ ic acids, myoglobin and nucleosides are all released into the circulation. Severe hyperkala emia may lead to cardiac dysrhythmias and even cardiac arrest, particularly in association with severe hypocalcaemia and acidosis. 503 CHAPTER 29.3 Rhabdomyolysis Table 29.3.2. Management of rhabdomyolysis Early or late complications Compartment syndrome may occur either early or later in the cou rse of rhabdomyolysis and may be exacerbated by hypotension. Fluid sequestration occurs and , as most mus- cles are within rigid compartments, this oedema leads to a rise in compartme nt pressure and impaired perfusion (compartment syndrome). Compartment pressures >30mm Hg p roduce clinically signi \201 cant muscle ischaemia and secondary rhabdomyolysis. Prolonged pressure may also lead to nerve damage. 1. Obtain immediate IV access and start isotonic saline 500ml/h then titrate to maintain a urine output of 200 \200\223300ml/h 2. Consider CVP monitoring (elderly, presence of cardiac failure, renal failure) 3. Treat any underlying conditions where indicated 4. Add IV sodium bicarbonate and titrate to urinary pH >6.5 where metabolic acidosis and/or hyperkalaemia are present 5. Consider I V mannitol (test dose of 200mg/kg IV over 3 \200\2235min to ensure adequate renal function, then 10ml/h) Late complications DIC may develop following rhabdomyolysis, usually >72h following injury. Acute renal failure is the most serious complication, developing in 16.5% of patients. It results from a combination of renal vasoconstriction, hypovolaemia, mechanical obstruction by intraluminal cast formation and direct cytotoxicity from the haem moiety of myoglobin. I n the presence of low urine \202 ow rates and low urinary pH, myoglobin interacts with Ta mm \200\223Horsfall protein and precipitates, causing obstructive cast formation. Hyper- ur icaemia and urinary excretion of uric acid exacerbate tubular obstruction through formation of uric acid casts. Degradation of precipitated myoglobin initiates lipid per- oxidation a nd renal injury, and release of free iron catalyzes free radical production and further enh ances ischaemic damage. During recovery, hypercalcaemia may occur. Calcium that has accumul ated in muscles at the time of initial muscle necrosis is released from storage sites durin g recovery, and this is enhanced if calcium supplementation has been administered during th e hypocalcaemic stage This can be associated with hyperparathyroidism and hypervitaminosis D in some cases, leading to overt hypercalcaemia. 6. Monitor for, and treat, complications 7. Repeat CK assay to determine peak CK level 8. C onsider fasciotomy in compartment syndrome Compartment syndrome Delay in management of compartment syndrome can lead to irreversible m uscle and nerve damage. Neurological symptoms and signs may indicate the need for fasciotom y, but measurement of intramuscular pressure provides an objective guide. Pressures consist ently exceeding 30mm Hg with no tendency to reduce are a clear indication. Renal replacement therapy Where acute renal failure is established, or in the presence of s evere hyperkalaemia and acidosis, RRT may be required. Fluid overload is rarely an indicati on for RRT in rhabdomy- olysis. Haemodialysis offers distinct advantages through its greate r ef \201 ciency and lack of need for continuous antico- agulation. Peritoneal dialysis is the least desirable mode of RRT in patients with rhabdomyolysis due to inef \201 ciency a nd dif \201 culties with administration. Adjuvants Free radical scavengers and antioxidants and dantrolene sodium have all been used experimentally, but do not yet have a proven clinical role. Management of rhabdomyolysis Initial stabilization and resuscitation, and prevention of acu te renal failure As much as 10 \200\22312l of \202 uid may be sequestrated in dam- aged m uscle, and IV hydration should be started as early as possible (Table 29.3.2). In patients with crush injury, this means implementation of IV therapy even whilst the patient is still trapped. The longer it takes for rehydration to be initiated, the more likely it is that a cute rebal failure will supervene. Further reading Akmal M, Massry S. Reversible hepatic dysfunction associated with rhabdomyolysis. Am J Nephrol 1990; 10: 49 \200\22352. Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in tr aumatic rhabdomyolysis. N Engl J Med 1990; 322: 825 \200\2239. Brown C, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: d o bicarbonate and mannitol make a differ- ence? J Trauma 2004; 56: 1191 \200\2236. Rationale for mannitol and bicarbonate therapy Mannitol is said to increase renal blood \202 ow and the GFR, potentially suck \202 uid out of the interstitial compartment reduci ng muscle swelling and thus risk of compartment syndrome, promote a diuresis and prevent pr ecipitation of obstructive tubular casts, and serve as a free radical scavenger. Bicarbonat e therapy is said to correct acidosis, reduces risk of hyperkalaemia and increases urinary pH, preventing pre- cipitation and degradation of myoglobin in the urinary tubules. Both ma nnitol and bicarbonate therapy are standard therapy, but neither has been subject to clinic al trials. Observational data suggest that they provide no additional bene \201 t over and above volume expansion with saline. Addition of mannitol and bicarbonate had no impact on development of acute renal failure, need for dialysis or mortality. Gabow PA, Kaehny WD, Kelleher SP. The spectrum of rhabdomy- olysis. Medicine (Baltimore) 1982; 61: 141 \200\22352. Knochel JP. Mechanisms of rhabdomyolysis. Curr Opin Rheumatol 1993; 5: 725 \200\22331. Lane JT, Boudreau RJ, Kinlaw WB. Disappearance of muscular cal- cium deposits during resolu tion of prolonged rhabdomyolysisin- duced hypercalcemia. Am J Med 1990; 89: 523 \200\22325. Orrell RW, Lane RJM. Myoglobinuria. In: Lane RJM, ed. Handbook of muscle disease. New York: Marcel Dekker, 1996: 607 \200\22311. Ward MM. Factors predictive of acute renal failure in rhabdomyoly- sis. Arch Intern Med 1988; 148: 1553 \200\2237. Zager RA. Rhabdomyolysis and myohemoglobinuric acute renal failure. Kidney Int 1996; 49: 314 \200\2232. 504 C THEAKER Pressure sores \200 \200 Introduction Pressure sores are a hazardous complication of ICU. They are de \201 ned as a n area(s) of local tissue damage caused by pressure, shear, moisture and friction or a comb ination thereof. The incidence of pressure sores within the inten- sive care population has been reported to be between 3 and 29%. They are also expensive and can cost up to 40 000 to treat. They can appear anywhere on the body. They act as a reservoir for microorganisms and are often extremely painful. For reasons not yet clear, medical staff often leave the entire problem to nursing staff; a team approach must be adopted. Medications Age Diabetes Achieving correct protein and calorific intake of ICU patients is particularly problematic. Tube feeding or TPN is often instigated despite their inherent risks. Knowing the patients weight is important as it allow the calculation of calori \201 c input. The European Pres sure Ulcer Advisory Panel (EPUAP) recommends that 30 \200\22335kcal/kg body weight per day, with 1 \200\2231.5g/kg/day protein required and 1ml/kcal/day of fluid intake serve as a mi nimum requirement. A common mistake is to overlook the patient \200\231s bowel sta- tus. If the patient is suffering from perfuse diarrhea, then it is unlikely that they will be abso rbing their nutritional needs despite the calculation being correct. Low serum albumin leve ls (<3.5g/dl) has been associated with an increase risk in pressure sore development. The p itfall here is to give IV albumin, raise the level and then assume the patient is no longer at risk. The correct approach is to treat the cause of the low serum albumin. Identi \201 cation Identi \201 cation of those at risk is problematic. Current scor- ing systems that attempt to identify patients at risk on ICU are often derivatives of those dev eloped for ward patients. Their effectiveness is unclear. All have the ability to over- or underestimate the risk of pressure sore development. They must be used in conjunction with clinical judgment. Common scoring systems include: \200 \200 \200 Waterlow Norton Braden Prevention In the ICU the most frequent method of prevention is a specialist bed or mattres s. These have cost implications. There are also many different types, but all aim to: \200 \200 Risk factors General Exposure either on one or more occasion to the forces of friction, she ar and pressure in the following context: \200 Provide a comfortable surface Redistribute pressure Pressure occurs when the patient \200\231s weight on a support surface causes body tissue t o become compressed against a bony prominence, resulting in poor capillary perfusion. Shear is the result of horizontal forces perpendicular to pressure, and is usually the end resul t of a combination of friction and movement. A common example of this occurs when a patient is sitting upright in bed but slides down, causing the sacral area to \200\230shear \200 \231. Friction occurs when two surfaces (usually the patient \200\231s skin and bed surface ) move against each other in opposition. The redistribution of pressure is achieved by either one of two methods: \200 \200 Pressure-reducing Pressure-relieving An example of a pressure-reducing mattress is the stand- ard hospital mattress. It reduces peak interface pressures by maximizing skin contact. It is of little use in very heavy pati ents \200\224a specialist mattress will be required. A pressure- relieving mattress has the aim of removing all pressure. This is done in either of two ways: \200 By suspending or raising vulnerable areas of the body by de \202 ating special cells built into the mattress. By timed in \202 ation and de \202 ation of air- \201 lled cells. ICU patients are generally at greater risk of pressure sore development due to prolonged pe riods of inactivity. The latter method uses 5 \200\22310min cycles provided by a pump that is often located at t he end of a patient \200\231s bed. Time cycles are of extreme importance, but optimal time cycles are dif \201 cult to achieve as the patient \200\231s condition changes. Speci \201 c In one study of 283 ICU patients, the following risk factors were found to be signi \201 cant in the development of pres- sure sores on ICU: \200 \200 \200 \200 \200 Anemia Noradrenaline infusion APACHE II score >13 upon admission Fecal incontinence Length of stay >3 days Other forms of prevention Frequent turning and repositioning (condition allowing) of the pa tient must be implemented even if they are on a pressure0relieving/reducing mattress. An un scienti \201 c 2- hourly turning regime is often quoted, but in all probability the freque ncy is proportionate to patient risk. Treating the patient \200\231s underlying condition, addressing die- tary requirements (the involvement of a dietician is manda- tory), correcti ng of anemia and early mobilization also fall into this category of prevention. Other A plethora of intrinsic factors exist that usually exacerbate the condition. They inc lude: \200 \200 \200 \200 \200 Poor dietary intake Steroids General health Weight Continence Grading Several grading systems attempt to classify the extent and nature of a pressure sor e. One of the better ones is that 505 CHAPTER 29.4 Pressure sores recommended by EPUAP. Pressure sores are graded into 4 types: \200 viability or wound care expert is mandatory. A positive wound swab will need the involvemen t of the microbiol- ogy team. There will be a difference as to whether the identi \201 ed organism(s) are either \200\230colonizing \200\231 or \200\230infecting \200\231 the woun d. An unnecessarily aggressive attempt to remove the organism(s) may result in delayed woun d healing. Grade 1 \200\224non-blanchable erythema of intact skin. Discoloration, warmth, induration o r hardness of skin may also be used as indicators, particularly in people with darker skin. Grade 2 \200\224partial thickness skin loss, involving the epidermis, dermis or both. The ulcer is super \201 cial and presents clinically as an abrasion or blister. Grade 3 \200 \224full thickness skin loss involving damage to or necrosis of subcutaneous tissue that ma y extend down to, but not through, underlying fascia. Grade 4 \200\224extensive destruction , tissue necrosis or dam- age to muscle, bone or supporting structures, with or without ful l thickness skin loss. Wound healing There are 3 distinct stages of wound healing: \200 \200 \200 In \202 ammatory Proliferation Maturation and remodeling The initial in \202 ammatory stage lasts usually only for a few days. Blood vessels are co nstricted to minimize loss of blood; platelets and thromboplastin attend the affected area in an effort to form a clot. White cells then enter the area to clear it of organisms and d ebris. This process gen- erates heat and redness which can be seen and felt at the wound si te. Depending on the severity of the pressure sore, the next stage of proliferation lasts f or 3 weeks. Fibroblasts attend the area to make collagen. Collagen \200\230 \201 lls \200\231 in the wound and is assisted signi \201 cantly by the forma- tion of new blood ve ssels. The \201 nal stage of maturation and remodeling is the most protracted. It can tak e up to 2yrs to complete. A new form of collagen arrives and attempts to re-mold and streng then the wound site. Scar tissue develops which although visibly appears stronger is, in fa ct, only 75% as strong as normal tissue. There is a particular problem associated with chro nic wounds in that the scar tissue cells can become unrespon- sive to growth markers and cy tokines, thereby prolonging the above stages and delaying healing considerably. Frequent assessment and documentation of the pressure sore using this scale is mandatory in order to track wound progress. A pressure sore can be likened to an iceberg in that despit e the appearance of slight skin damage on the skin surface, the dermis and epidermis may ha ve considerable damage. Any area of redness is a cause for concern. Pressure sores can deve lop as a result of the use of equipment. Pressure sores developing on the bridge of patient \200\231s noses from CPAP masks is not uncommon, and have been the subject of successful l itigation. Ventilator tubing, abandoned ven \202 on bungs, drip and drain tubing, ECG dots and monitor wiring serve as other examples. Wound treatment ICU patients seem particularly vulnerable to developing pressure sores on t heir heels. If a pressure sore develops it will require treatment. Wound treatments exist t hat range from wound cleaning to surgical debridement. Grade 1 pressure sores seldom requir e pharmaceutical or surgical treatment, but for the other grades an expanse of creams, gels , pads, dressings and devices exist. Treatment is largely governed by the nature, location and type of pres- sure sore. In general: \200 Conclusion The following serve as an aide memoir to the successful management of pressure s ores: \200 \200 Do not use sheep skins, they do not work Do not leave pressure sores to nursing staff; you have a part to play Inspect skin areas frequently, particularly the sacrum and the heels. D ocument, and if necessary photograph, any pressure sores Ensure regular reviews of the pati ent \200\231s risk factors are performed Regularly inspect any pressure sores that develop Treat pressure sores appropriately; quality advice can be obtained from your local Tissue V iability Nurse. Dressings should not \200\230dry \200\231 the wound but maintain a moist environment. Do n ot use systemic antibiotics in an attempt to eradi- cate bacteria within the wound. Frequen t removal of dressings could disturb the wound- healing process \200\230Hard \200\231 dres sings or pads should not be used as they can exacerbate pressure. Handwashing and other inf ection control measures must be adopted to prevent wound contamination or bacte- rial sprea d. Dressings should remain in place as in accordance with the manufacturer \200\231s recomm endations. \200 Further reading Theaker C, Mannan M, Ives N, et al. Risk factors for pressure sores in the critically ill. Anesthesia 2000; 55: 221 \200\2234. A large \200\230custom and practice \200\231 culture exists around the treatment of pressu re sores. Expert advice from a tissue This page intentionally left blank 507 Chapter 30 Pain and post-operative intensive care Chapter contents Pain management in ICU 508 Intensive care for the high risk surgical patie nt 510 The acute surgical abdomen in the ITU 512 The medical patient with surgical problems 514 508 CS WALDMANN Pain management in ICU Introduction Relief from pain is not only indicated on humanitarian and ethical grounds alo ne, but has medical and possibly cost bene \201 ts. and their stay on ICU. In order to minimize this time, daily sedation holding is now a feat ure of the \200\230ventilator \200\231 bundle of care. The use of early percutaneous trach eostomy may also be a means of reducing weaning times. Before resorting to hypnotic-based r egimes for sedation, it is important that the patient is assessed regularly for pain and ad equately treated. Patients \200\231 requirements for strong anal- gesic drugs may be modi \201 ed or reduced by attention to: \200 \200 \200 \200 \200 Terminology \200 Oxford dictionary \200\224sensation of physical suffering or acute discomfort The Internati onal Association for the Study of Pain 1986 \200\224 an unpleasant sensory and emotional ex perience associ- ated with actual or potential tissue damage or described in terms of such damage Neuropathic pain \200\224seen in patients in the ICU due to nerve damage, herpes zos ter, GBS; does not respond to conventional analgesics but may require combinations of drugs such as amitryptylline, carbemazepine, sodium val- proate, gabapentin and ketamine. Reduce noise levels Change pulse oximeter \201 nger regularly Reduce \202 atulence, nau sea Immobilize fractures Establish sleep pattern Despite ICU staff believing that pain is adequately treated, many studies have shown that a t least 50% of ICU patients experienced moderate or severe pain during their ICU stay, and the CoBATRICE patient and relatives survey dem- onstrated that 76% of responders expected i ntensive care staff to do everything to control pain. The use of analgesia-based sedation w as described by Lane et al. in 2002, and has been responsible for a trend in the reduction of hypnotic-based regimes. There are concerns with hypnotic-based regimes particularly sinc e 1984 when it was discovered that etomidate was associated with ade- nal gland suppression and increased mortality in trauma patients. However, it is only recently in 2005 that the con- tinued use of etomidate has been questioned. There is literature to demonstrate that p ropofol in chil- dren and in adults with head injury can be associated with an excess morta lity. Causes of pain in ICU patients \200 \200 \200 \200 \200 \200 Post-surgery Trauma Organ dysfunction: gut ischaemia, DVT, cardiac Treatment: procedures on ICU, change of dressings Pre-existing pain: vascular, neuropathic, rheumatoid Pain of term inal disease. Adverse effects of pain \200 Respiratory: atelectasis \200 Cardiovascular: stress, MI \200 Gut: ileus, nausea, vomiting \200 Genitourinary: retention, agitation \200 Endocr ine: increased ADH, water retention \200 Hematological: venous stasis, DVT \200 Musculo skeletal: immobility, critical illness polyneuropa- thy and myopathy, pulse oximeter probe Neuropsychological: decreased sleep, agitation, delirium, post-traumatic stress disorder. Guidelines The Fundamentals of the Critical Care Support (FCCS) manual outlines the use of drugs such as lorazepam, mor- phine and fentanyl for analgesia and sedation, and empha- siz es the importance of not using these drugs as a method of restraint by staff (Federal Regul ation 42 CFR 482.13), but points out that where it is thought that pain is the cause of agi tation, then analgesia would be the appropriate initial therapy. The Intensive Care Society Guidelines state that: \200 All patients must be comfortable and painfree \200 Anxiety should be minimized \200 Patients sould be calm, cooperative and able to sleep \200 Pa tients should tolerate organ system support and be able to synchronize with ventilator Pati ents must not be paralyzed and awake Assessment of pain in ICU \200 \200 \200 