See also: Anticoagulants, p318; Thrombolytics, p320; Acute coronary syndrome (1), p388; Acu te coronary syndrome (2), p390. This page intentionally left blank 107 Chapter 4 Renal therapy techniques Haemo(dia) \201 ltration (1) 108 Haemo(dia) \201 ltration (2) 110 Peritoneal dialysis 112 Plasma exchange 114 108 CHAPTER 4 Renal therapy techniques Haemo(dia) \201 ltration (1) Conventional haemodialysis requires a pressurized, puri \201 ed water supply, and a greater risk of haemodynamic instability due to rapid \202 uid an d osmotic shifts. Haemo(dia) \201 ltration can be arterio-venous, using the patient \200 \231s BP to drive blood through the haemo \201 lter, or pumped veno- venous. The latter is preferable as it does not depend on the patient \200\231s BP, and the pump system incorpor ates alarms and safety features. Continuous veno-venous haemo(dia) \201 ltration (CVVH or CVVHD) is increasingly the technique of choice. Blood is usually drawn and returned via a 1 0 \200\22312Fr double-lumen, central venous catheter (see \201 gure 4.1). Indications \200 \200 \200 \200 \200 \200 \200 Azotaemia (uraemia). Hyperkalaemia. Anuria/oliguria; to make space for nutrition. Severe me tabolic acidosis of non-tissue hypoperfusion origin. Fluid overload. Drug removal. Hypother mia/hyperthermia. Techniques CVVH relies on convection (bulk transfer of solute and water) to clear solute. I n CVVHD, dialysate \202 ows countercurrent to the blood, allowing small mol- ecules to di ffuse according to their concentration gradients. Membranes are usually hollow \201 bre polyacrylonitrile, polyamide, or polysulphone with a surface area of 0.6 \200\2231m2. Both CVVH and CVVHD are effective for small molecule clearance (e.g. urea). CVVH is better at larger molecule clearance and can remove substances up to the membrane pore size cut-off (usually 30 \200\22335kD). Filtrate is usually removed at 20 \200\22335mL/kg/h; \202 uid balance is adjusted by varying the rate of \202 uid replacement. High volume haemo \201 ltration involves much higher ultra \201 ltration rates (e.g. 50 \200\223100mL/kg/h, usua lly for short periods, e.g. 4h) in an effort to remove in \202 ammatory mediators. Variabl e outcomes are reported in studies. Creatinine and K+ clearances are higher with CVVHD, but \201 ltration alone is usually su f \201 cient if ultra \201 ltrate volume is adequate. (1000mL/h approximates to a creatin ine clearance of 16mL/min). CVVHD is preferred for pharmacologically-resistant hyperkalaemi a. Replacement \202 uid A balanced electrolyte solution buffers acidaemia and is titrated to desired \202 uid and electrolyte balance. Buffers include lactate (liver metabolized to bicarbonate) and bicarbonate. Acetate (metabolized by muscle) causes most haemodynamic inst ability and is now rarely used. Bicarbonate may be more ef \201 cient than lactate at reve rsing severe acidosis, but no outcome bene \201 t has been shown. Care is needed when givi ng Ca2+ since calcium bicarbonate may crystallize. In hypoperfused liver, lactate may be in ade- quately metabolized. Increasing metabolic alkalosis may be due to excessive buffer so use low buffer (30mmol/L l actate) replacement \202 uid. K+ can be added to maintain normokalaemia. 20mmol KCl in a 4.5L bag provides a concentra- tion of 4.44mmol/L. K+ clearance is increased by reducing th e concentra- tion within replacement \202 uid or dialysate. HAEMO(DIA)FILTRATION (1) 109 HAEMOFILTRATION Replacement fluid Anticoagulant Convection + solvent drag + ultrafiltration Blood to patient Blood from patient Ultrafiltrate HAEMODIAFILTRATION Replacement fluid Anticoagulant Diffusion + ultrafiltration Blood to patient Blood from patient Dialysis fluid Dialysate + ultrafiltrate Fig. 4.1 Circuit arrangement for haemo(dia) \201 ltration. Key papers Ronco C, Bellomo R, Homel P, et al. (2000) Effects of different doses in continu ous veno-venous haemo \201 ltration on outcomes of acute renal failure: a prospective rand omized trial. Lancet 356: 26 \200\22330. Bouman CS, Oudermans-Van Straaten HM, et al. (2002) Effects of early high-volume continuous venovenous haemo \201 ltration on survival and recovery of renal function in intensive ca re patients with acute renal failure: a prospective, randomized trial. Crit Care Med 30: 22 05 \200\22311. The VA/NIH Acute Renal Failure Trial Network. (2008) Intensity of renal support in critical ly ill patients with acute kidney injury. N Engl J Med 359: 7 \200\22320. See also: Haemo(dia) \201 ltration (2), p110; Oliguria, p398; Acute renal failure \200\224 diagnosis, p400; Acute renal failure \200\224management, p402. 110 CHAPTER 4 Renal therapy techniques Haemo(dia) \201 ltration (2) Anticoagulation The circuit can be anticoagulated with unfrac tionated heparin (200 \200\2232000IU/h), a prostanoid (prostacyclin or PGE1) at 2 \200\2231 0ng/kg/min, or a combination of the two. Other alternatives include regional citrate antico agulation, the low molecular weight heparinoid danaparoid, or direct thrombin inhibi- tors (e.g. lepirudin, argatroban). These agents are, as yet, under-evaluated for renal replaceme nt therapy and they risk important complications such as hypocalcaemia (with citrate) and p rolonged bleeding with the long half-lives of the thrombin inhibitors. Bivalirudin is a new agent related to hirudin and lepirudin but is reversible with a short half-life of only 25 min. No anticoagulant may be needed if the patient is auto-anticoagulated. Premature clotting may be due to mechanical kinking/obstruction of the circuit, insuf \201 cient anticoagulation, inadequate blood \202 ow rates, or lack of endogenous anticoagula nts such as antithrombin III. Usual \201 lter lifespan should be at least two days, but is often decreased in septic pa tients due to decreased endogenous anticoagulant levels. In this situation, consider use of fresh frozen plasma, a synthetic protease inhibitor such as aprotinin, or antithrombin III replacement (costly). Filter blood \202 ow Flow through the \201 lter is usually 100 \200\223200mL/min. Too s low a \202 ow rate promotes clotting. Too high a \202 ow rate will increase transmembra ne pres- sures and decrease \201 lter lifespan without signi \201 cant improvement in cl ear- ance of \200\230middle molecules \200\231 (e.g. urea). Complications \200 \200 \200 Disconnection leading to hemorrhage. Infection risk (sterile technique must be employed). E lectrolyte, acid-base or \202 uid imbalance (due to excess input or removal). Hemorrhage (vascular access sites, peptic ulcers) related to anticoagulation therapy or consumption co agulopathy. Heparin-induced thrombocytopaenia may rarely occur. Cautions \200 \200 \200 \200 \200 \200 \200 Haemodynamic instability related to hypovolaemia (especially at start). Vasoactive drug rem oval by the \201 lter (e.g. catecholamines). Membrane biocompatibility problems (especial ly with cuprophane). Drug dosages may need to be revised (consult pharmacist). Amino acid l osses through the \201 lter. Heat loss leading to hypothermia. Masking of pyrexia. HAEMO(DIA)FILTRATION (2) 111 See also: Haemo(dia) \201 ltration (1), p108; Coagulation monitoring, p222; Anticoagulants , p318. 112 CHAPTER 4 Renal therapy techniques Peritoneal dialysis A slow form of dialysis, utilizing the peritoneum as the dialysis membr ane. It is now rarely used in UK Critical Care Units, having been largely super- seded by c ontinuous haemo \201 ltration. The technique does not require complex equipment although c ontinuous \202 ow techniques do require con- tinuous generation of dialysate. Treatment i s labor-intensive and there is considerable risk of peritoneal infection. Peritoneal access For acute peritoneal dialysis, a trochar and cannula are inserted through a small skin incision under local anesthetic. The skin is prepared and draped as for any s terile procedure. The commonest approach is through a small midline incision 1cm below the umbilicus. The subcutaneous tissues and peritoneum are punctured by the trocar which is wit hdrawn slightly before the cannula is advanced towards the pouch of Douglas. In order to av oid damage to intra- abdominal structures, 1 \200\2232L warmed peritoneal dialysate may be infused into the peritoneum by a standard, short intravascular cannula prior to placement o f the trocar and cannula system. If the midline access site is not available, an alternativ e is to use a lateral approach, lateral to a line joining the umbilicus and the anterior su perior iliac spine (avoiding the inferior epigastric vessels). Dialysis technique Warmed peritoneal dialysate is infused into the peritoneum in a volume o f 1 \200\2232L at a time. During the acute phase, \202 uid is \202 ushed in and drained con- tinuously (i.e. with no dwell time). Once biochemical control is achieved, it is usua l to leave \202 uid in the peritoneal cavity for 4 \200\2236h before draining. Heparin (5 00IU/L) may be added to the \201 rst six cycles to prevent \201 brin catheter blockage. Thereafter, it is only necessary if there is blood or cloudiness in the drainage \202 ui d. Peritoneal dialysate The dialysate is a sterile balanced electrolyte solution with glucose at 75mmol/L for a standard \202 uid or 311mmol/L for a hypertonic \202 uid (used for gr eater \202 uid removal). The \202 uid is usually potassium-free since potas- sium excha nges slowly in peritoneal dialysis although potassium may be added if necessary. Complications \200 Fluid leak Poor drainage Corticosteroid therapy Obese or elderly patient Bleeding Omental encasement W hite cells >50/mL, cloudy drainage \202 uid Absorption of hyperosmotic glucose Catheter blockage \200 \200 Infection Hyperglycaemia Diaphragm splinting Treatment of infection It is possible to sterilize the peritoneum and catheter by adding ap pro- priate antibiotics to the dialysate. Suitable regimens include: \200 \200 Cefuroxime 500mg/L for two cycles, then 200mg/L for 10d. Gentamicin 8mg/L for one cycle dai ly. PERITONEAL DIALYSIS 113 See also: Oliguria, p398; Acute renal failure \200\224diagnosis, p400; Acute renal failure \200\224management, p402. 114 CHAPTER 4 Renal therapy techniques Plasma exchange Indications Plasma exchange may be used to remove circulating toxins or to replace missing plasma factors. It may be used in sepsis (e.g. meningococcaemia). In patien ts with immune mediated disease (e.g. Guillain \200\223Barr syndrome, thrombotic thromboc ytopaenic purpura), plasma exchange is usually a temporary measure while systemic immunosup pression takes effect. Most diseases require a daily 3 \200\2234L plasma exchange repeated for at least four further occasions over 5 \200\22310 days. Techniques Cell separation by centrifugation Blood is separated into components in a centri fuge. Plasma (or other spe- ci \201 c blood components) is discarded and a plasma replacem ent \202 uid is infused in equal volume. Centrifugation may be continuous (where blood is withdrawn and returned by separate needles) or intermittent (where blood is withdrawn and separated, then returned via the same needle). Membrane \201 ltration Plasma is continuously \201 ltered through a large pore \201 l ter (molecular weight cut-off typically 1,000,000D). Plasma is discarded and replaced by in fusion of an equal volume of replacement \202 uid. The technique is similar to haemo \201 ltration and uses the same equipment. Replacement \202 uid Most patients will tolerate replacement with a plasma substitute. So me fresh frozen plasma will be necessary after the exchange to replace coag- ulation factor s. The only indication to replace plasma loss with all fresh frozen plasma is where plasma exchange is being performed to replace missing plasma factors. Complications \200 Circulatory instability Intravascular volume changes Removal of circulating catecholamines Hypocalcaemia If replace ment with crystalloid Reduced plasma opsonisation Removal of coagulation factors \200 \200 Reduced intravascular COP Infection Bleeding PLASMA EXCHANGE 115 Indications Autoimmune disease Goodpasture \200\231s syndrome Guillain \200\223Barr syndrome Myasthenia gravis Pemphigus Rapidly progressive glomerulonephritis Systemic lupus erythematosus Thrombotic thrombocytopaenic purpura Immunoproliferative disease Cryoglobulinaemia Multiple myeloma Waldenstrom \200\231s macroglobulinaemia Poisoning Paraquat Others Meningococcaemia (possible bene \201 t) Sepsis (possible bene \201 t) Reye \200\231s syndrome See also: Guillain Barr syndrome, p456; Myasthenia gravis, p458; Platelet disorders, p478 ; Vasculitides, p574. This page intentionally left blank 117 Chapter 5 Gastrointestinal therapy techniques Sengstaken-type tube 118 Upper gastrointestinal endoscopy 120 Enteral feeding and drainage tubes 122 118 CHAPTER 5 Gastrointestinal therapy techniques Sengstaken-type tube Used to manage oesophageal variceal hemorrhage that continues despite pharmacological 9 per-endoscopic therapy. The device (Sengstaken \200\223 Blakemore or simi lar) is a large-bore rubber tube, usually containing two balloons (oesophageal and gastric) and two further lumens (oesophageal and gastric) that open above and below the balloons. T his device works usually by the gastric balloon alone compressing the varices at the cardia . In \202 ation of the oesophageal balloon is rarely necessary. Insertion technique The tubes are usually kept in the fridge to provide added stiffness for easier insertion. 1. The patient often requires judicious sedation or mechanical ventilation (as warranted by co nscious state/level of agitation) prior to insertion. Check balloons in \202 ate properly beforehand. Lubricate end of tube. Insert via mouth. Place to depth of 55 \200\22360cm, i.e . to ensure gastric balloon is in stomach prior to in \202 ation. In \202 ate gastric bal loon with water to volume instructed by manufacturer (usually 200mL). A small amount of rad io-opaque contrast may be added. Negligible resistance to in \202 ation should be felt. Cl amp gastric balloon lumen. Pull tube back until resistance is felt, i.e. gastric balloon is at cardia. Fix tube in place by applying countertraction at the mouth. Old- fashioned meth ods, such as attaching the tube to a free-hanging liter bag of saline, have been superseded by more manageable techniques. For example, two wooden tongue depressors, \200\230thicken ed \200\231 by having Elastoplast wound around them, are placed on either side of the tub e at the mouth and then attached to each other at both ends by more Elastoplast . The tube remains gripped at the mouth/cheek by the attached tongue depressors, but can be retracted until adequate but not excessive traction is being applied. Perform X-ray to check satisfa ctory position of gastric balloon. If bleeding continues (continued large aspirates from ga stric or oesophageal lumens), in \202 ate oesophageal balloon (approximately 50mL). 2. 3. 4. 5. 6. 7. Subsequent management 1. The gastric balloon is usually kept in \202 ated for 12 \200\22324h and de \202 ated prio r to endoscopy 9 sclerotherapy. The traction on the tube should be tested hourly by the nur sing staff. The oesophageal lumen should be placed on continuous drainage while enteral nut rition and administration of drugs can be given via the gastric lumen. If the oesophageal b alloon is used, de \202 ate for 5 \200\22310min every 1 \200\2232h to reduce the risk of o esophageal pressure necrosis. Do not leave oesophageal balloon in \202 ated for >12h after sclerotherapy. The tube may need to stay in situ for 2 \200\2233d though periods of de \202 ation should then be allowed. 2. 3. Complications \200 Aspiration. \200 Perforation. \200 Ulceration. \200 Oesophageal necrosis. SENGSTAKEN-TYPE TUBE 119 See also: Upper gastrointestinal hemorrhage, p412; Bleeding varices, p414. 120 CHAPTER 5 Gastrointestinal therapy techniques Upper gastrointestinal endoscopy Oesophago-gastro-duodenoscopy is performed identically in ventilated and non-ventilated patients. Additional sedation may be needed, especially if th e patient is awake and/or agitated. A protected airway facilitates the procedure and also o ffers additional safety if the patient \200\231s conscious level if obtunded, and there is a high risk of aspiration of gastric contents (blood or food/liquid if ileus or obstruction is present). Indications \200 Investigation of upper GI signs/symptoms. e.g. bleeding, pain, mass, obstruction. Therapeut ic, e.g. sclerotherapy and/or banding for varices, local epinephrine (adrenaline) injection or heat probe (thermocoagulation) for discrete bleeding points, e.g. in peptic ulcer base. Placement of nasojejunal tube (when gastric atony prevents enteral feeding) or percutaneou s gastrostomy (PEG). ERCP \200\224relatively unusual in the ICU patient but may be needed f or bile duct/pancreatic duct obstruction. Complications \200 \200 \200 Local trauma causing hemorrhage or perforation. Abdominal distension with gas, compromising respiratory function. Aspiration of gastric contents. Contraindications/cautions \200 \200 Severe coagulopathy should ideally be corrected. Caution with upper GI tract pathology as r isk of perforation. Procedure Upper GI endoscopy should be performed by an experienced operator to minimize the duration and trauma of the procedure, and to minimize gaseous distension of the gut. 1. 2. The patient is usually placed in a lateral position. Increase FIO2 and ventilator pressure alarm settings. Consider increasing sedation and adjusting ventilator mode. Monitor ECG, Sp O2, airway pressures, and haemodynamic variables throughout. If patient is on pressure supp ort or pressure control ventilatory modes, also monitor tidal volumes. The operator should cease the procedure, at least temporarily, if the patient becomes compromised. At the end o f the procedure, the operator should aspirate as much air as possible out of the GI tract t o decompress the abdomen, and resite a nasogastric tube which often becomes displaced. 3. 4. UPPER GASTROINTESTINAL ENDOSCOPY 121 See also: Upper gastrointestinal hemorrhage, p412; Bleeding varices, p414. 122 CHAPTER 5 Gastrointestinal therapy techniques Enteral feeding and drainage tubes Types of tube Nasogastric Enteral tube routinely placed in critical care patients to provide nutrition and oral medication, or to drain/decompress the stomach. \200 Never use excessive force during insertion if tube does not pass smoothly. Due to external compression from the endotracheal tube, cuff, McGill forceps, or similar may aid passage th rough the pharynx in intubated patients (under laryngoscopic guidance). Before food, liquid , or drug administration, correct positioning of tip should be veri \201 ed by two of: asp iration of acidic \202 uid (pH <5), positive auscultation over gastric area when air is i njected, and radiological con \201 rmation. Auscultation is the least speci \201 c techni que and should not be relied upon alone. The tube should be tethered securely to the nose. In agitated patients, this may require a sling or suture, especially if repeatedly removed. Tube insertion depth should be recorded and regularly checked to ensure non-migration prox imally. A nasogastric tube is contraindicated if there is: \200 Any nasopharyngeal or upper GI pathology that obstructs lumen or increases risk of perforat ion/bleeding, unless expert advice is \201 rst obtained (e.g. ENT, GI specialist). Bleedi ng oesophageal varices (non-bleeding varices are not an absolute contraindication). Base of skull fracture. Severe coagulopathy. \200 Orogastric \200 \200 Sited if contraindication to nasal route, e.g. basal skull fracture. Otherwise, similar rul es as above apply to NG tube though it is dif \201 cult to securely tether and is less wel l tolerated by patient. Nasoduodenal/nasojejunal \200 \200 Used for gastric outlet obstruction or prolonged gastric ileus. Sited radiologically under endoscopic guidance or blind (a weighted tube migrates distally from the stomach over time) . Percutaneous enterogastrotomy (PEG)/jejunostomy (PEJ) Feeding tube inserted percutaneously under radiological or endoscopic guidance or by direct surgical placement. \200 Mainly used for long-term nutrition in patients who cannot maintain adequate oral intake, s uch as head and neck pathology (e.g. cancer), swallowing dif \201 culties (e.g. stroke, se vere head injury). The risk of aspiration pneumonia is reduced. Avoid in patients with seve re coughing. Correct coagulopathy before insertion (platelets >50x109/L and INR <1.5). Usua lly retained with an intraluminal balloon 9 attachment to skin. Follow local guidelines (an tibiotic prophylaxis, period of delay before use, initial introduction of water pre-feeding , site care, etc.). Such tubes carry a 3 \200\2238% morbidity rate and mortality <1% from i nfection, perforation, internal leakage, peritonitis, bleeding. \200 \200 \200 ENTERAL FEEDING AND DRAINAGE TUBES 123 See also: Enteral nutrition, p128; Vomiting/gastric stasis, p406. This page intentionally left blank 125 Chapter 6 Nutrition and metabolic therapy Nutrition \200\224use and indications 126 Enteral nutrition 128 Parenteral nutrition 130 Ti ght glycaemic control/intensive insulin therapy 132 126 CHAPTER 6 Nutrition and metabolic therapy Nutrition \200\224use and indications Malnutrition leads to an increased risk of infection due to immune compromise (related to decreased intake of trace elements, amino acids and vi tamins, plus decreased production of leptin), increased fatigability and inability to wean/ mobilize due to loss of muscle bulk, and poor wound healing. Gut mucosal atrophy occurs wit hin days of non-feeding and may compromise the ability to feed enterally. Adequate nutritional support should, in general, be provided early during critical illness. Improved outcomes from early nutritional support exist for patients with trauma and burns. Enteral feed is also a gastric pro- tectant. However, the patient should be resuscitated a nd stabilized before enteral feeding is contemplated as gut hypoperfusion will compromise t he ability to absorb, and feeding may render the gut more ischaemic. Increasing abdominal d istension, pain/discomfort, large gastric aspirates, and diarrhea suggest the need for a pe riod of bowel rest rather than persisting with feeding and addition of prokinetics. Enteral nutrition is indicated when swallowing is inadequate or impos- sible but GI functio n is otherwise intact. Parenteral nutrition is indi- cated when the GI tract cannot be used to provide adequate nutritional support, e.g. obstruction, ileus, high small bowel \201 stula, or malabsorption. Parenteral nutrition may be used to supplement enteral nutrition. Calorie requirements As with nitrogen requirements below, this is inexact and optimal day-t o- day intake is not known for individual patients. Various formulas can calcu- late basal metabolic rate but are misleading in critical illness. Metabolic rate can be measured by in direct calorimetry, but most patients are assumed to require 2000 \200\2232700Cal/d or less if starved or underweight. Burn-injured patients generally receive more feed. Nitrogen requirements Nitrogen excretion can be calculated in the absence of renal failure according to the 24h urea excretion. Nitrogen (g/24h) = 2 + urinary urea (mmol/24h) x 0.028 However, as with most formulas, this method lacks accuracy. Most patients require 7 \210 \22214g/d. Other requirements The normal requirements of substrates, vitamins, and trace elements are tabled opposite. Most long-term, critically ill patients require folic acid and vitamin sup plementation during nutritional support. Trace elements are usually supplemented in parente ral formulas but should not be required during enteral nutrition. NUTRITION \200\224USE AND INDICATIONS 127 Consequences of malnutrition Underfeeding Loss of muscle mass Reduced respiratory function Reduced immune function Poor wound healing Gut mucosal atrophy Reduced protein synthesis Overfeeding Increased VO2 Increased VCO2 Hyperglycaemia Fatty in \201 ltration of liver Normal daily requirements (for a 70kg adult) Water Energy Nitrogen Glucose Lipid Sodium Potassium Calcium Magnesium Phosphate Vitamins T hiamine Ribo \202 avin Niacin Pyridoxine Folate Vitamin C Vitamin A Vitamin D Vitamin E Vi tamin K 2100mL 2000 \200\2232700Cal 7 \200\22314g 210g 140g 70 \200\223140mmol 50 \200\223120mmol 5 \200\22310mmol 5 \200\22310mmol 10 \200\22320mmol 16 \200\22319mg 3 \200\2238mg 33 \200\22334mg 5 \200\22310mg 0.3 \200\2230.5mg 250 \200\223 450mg 2800 \200\2233300IU 280 \200\223330IU 1.4 \200\2231.7IU 0.7mg Trace elements Iron Copper Manganese Zinc Iodide Fluoride Additional requirements are neede d to satisfy excess loss or increased metabolic activity. 1 \200\2232mg 0.5 \200\2231.0mg 1 \200\2232mcg 2 \200\2234mg 70 \200\223140mcg 1 \200\2232m g See also: Enteral nutrition, p128; Parenteral nutrition, p130. 128 CHAPTER 6 Nutrition and metabolic therapy Enteral nutrition Routes include nasogastric, nasoduodenal/jejunal, gastrostomy, and jejuno stomy. Nasal tube feeding should be via a soft, \201 ne-bore tube to aid patient comfort and avoid ulceration of the nose or esophagus. Prolonged enteral feeding may be accomplishe d via a percutaneous/per-operative gastrostomy or jejunostomy. Enteral feeding provides a m ore complete diet than parenteral nutrition, maintains structural integrity of the gut, imp roves bowel adaptation after resection, and reduces infection risk. Feed composition Most patients tolerate iso-osmolar, non-lactose feed. Carbohydrates are pr ovided as sucrose or glucose polymers; protein as whole protein or oligopeptides (may be be tter absorbed than free amino acids in \200\230ele- mental \200\231 feeds); fats as medium chain or long chain triglycerides. Medium chain triglycerides are better absorbed. Standar d feed is formulated at 1Cal/mL. Special feeds are available, e.g. high \201 bre, high pr otein-calorie, restricted salt, high fat or concentrated (1.5 or 2Cal/mL) for \202 uid re stric- tion. Immune-enhanced feeds (e.g. glutamine-enriched or Impact , a feed supplemente d with nucleotides, arginine, and \201 sh oil) may reduce nosoco- mial infections, but no evidence of outcome bene \201 t has yet been shown from large prospective studies. Management of enteral nutrition Once a decision is made to start enteral nutrition, 30mL/h full strength standard feed may be started immediately. Starter regimens incorporating dilu te feed are not necessary. After 4h at 30mL/h, the feed should be stopped for 30min prior t o aspiration of the stomach. Since gastric juice production is increased by the presence of a nasogastric tube, it is reason- able to accept an aspirate of <200mL as evidence of gast ric emptying, and therefore, to increase the infusion rate to 60mL/h. This process is repea ted until the target feed rate is achieved. Thereafter, aspiration of the stomach can be re duced to 8-hourly. If gastric aspirate volume >200mL, the infu- sion rate is not increased though feed is continued. If aspirates remain at high volume, consider either prokinetics t o promote gastric emptying (e.g. metoclopramide, erythromycin), bowel rest (especially if a bdominal disten- sion or discomfort increases), nasoduodenal/jejunal or parenteral feeding. Complications \200 Tube misplacement: tracheobronchial, nasopharyngeal perforation, intracranial penetration ( basal skull fracture), oesophageal perforation. Re \202 ux. Pulmonary aspiration. Nausea a nd vomiting. Abdominal distension is occasionally reported with features including a tender , distended abdomen, and an increasing metabolic acidosis. Laparotomy and bowel resection m ay be necessary in severe cases. Refeeding syndrome. Diarrhea: large volume, bolus feeding, high osmolality, infection, lactose intolerance, antibiotic therapy, high fat content. Con stipation. Metabolic: dehydration, hyperglycaemia, electrolyte imbalance. \200 \200 \200 \200 \200 ENTERAL NUTRITION 129 Key paper Atkinson S, Sieffert E, Bihari D. (1998) A prospective, randomized, double-blind, controlled clinical trial of enteral immunonutrition in the critically ill. Crit Care Med 26: 1164 \200\22372. See also: Nutrition \200\224use and indications, p126; Gut motility agents, p294; Vomiting/ gastric stasis, p406; Diarrhea, p408. 130 CHAPTER 6 Nutrition and metabolic therapy Parenteral nutrition Feed composition Carbohydrate is normally provided as concentrated glu cose. 30 \200\22340% of total calories are usually given as lipid (e.g. soya bean emulsion) . The nitrogen source is synthetic, crystalline L-amino acids which should contain appropri ate quantities of all essential and most non-essential amino acids. Carbohydrate, lipid, an d nitrogen sources are usually mixed into a large bag in a sterile drugstore unit. Vitamins , trace elements, and appropriate electrolyte concentrations can be achieved in a single in fusion, thus avoiding multiple connections. Volume, protein and calorie content of the feed should be determined on a daily basis in conjunction with the dietician. Choice of parenteral feeding route Central venous A dedicated catheter (or lumen of a multi -lumen catheter) is placed under sterile conditions. For long-term feeding, a subcutaneous tunnel is often used to separate skin and vein entry sites. This probably reduces the risk of infection and clearly identi \201 es the special purpose of the catheter. Ideally, bloo d samples should not be taken nor other injections or infusions given via the feeding lumen . The central venous route allows infusion of hyper- osmolar solutions, providing adequate energy intake in reduced volume. Peripheral venous Parenteral nutrition via the peripheral route requires a solution with os molality <800mOsm/kg. Either the volume must be increased or the energy content (particular ly from carbohydrate) reduced. Peripheral cannulae sites must be changed frequently. Complications Catheter-related Misplacement Infection Thromboembolism Fluid excess Hyperosmolar, hyperglycaemic state Electrolyte imbalance Hypophosphataemia Met abolic acidosis Hyperchloraemia Metabolism of cationic amino acids Rebound hypoglycaemia (from high endogen ous insulin levels) Vitamin de \201 ciency Folate (pancytopaenia) Thiamine (encephalopathy, neuropathy, heart failure) Vitamin K (hypoprothrombinaemia) Vitamin A (dermatitis) Vitamin D (hypercalcaemia) Vitamin excess Fatty liver PARENTERAL NUTRITION 131 See also: Nutrition \200\224use and indications, p126; Indirect calorimetry, p234; Electrol yte management, p482; Hypophosphataemia, p498; Metabolic acidosis, p502; Hyperglycaemia, p5 08. 132 CHAPTER 6 Nutrition and metabolic therapy Tight glycaemic control/intensive insulin therapy Rationale Hyperglycaemia and insulin resi stance occur commonly in critically ill patients and are associated with an increased risk of mortality. This may be related to immune compromise, an increased rate of bacterial grow th, and the effects of glycation and free radical production on protein, lipid and mitochon drial function and integrity. In two landmark papers by van den Berghe et al., a combination of tight glucose control (ai ming for blood glucose levels of 4.5 \200\2236.1mmol/L) plus additional glucose and insulin administration reduced mortality and mor- bidity in both surgical and medical critical car e patients. Bene \201 t was only seen in those receiving >3 \200\2234 days \200\231 therap y. Controversy has since existed regarding how tight the glucose control should be, with some advocating a 5 \200\2238mmol/L target range to reduce the risk of potentially injurious hyp oglycaemia, particularly as regular testing introduces a signi \201 cant nurse workload. T he introduction of (semi-) con- tinuous, (semi-) automated blood glucose monitoring devices should facili- tate closer maintenance of normoglycaemia. Protocol Several protocols and algorithms have been devised by different groups. None are p erfect, but suit the particular circumstances of their units in terms of staf \201 ng leve ls and expertise. TIGHT GLYCAEMIC CONTROL/INTENSIVE INSULIN THERAPY 133 Key papers Van den Berghe G, Wouters P, Weekers F, et al. (2001) Intensive insulin therapy in critically ill patients. N Engl J Med 345: 1359 \200\22367. Van den Berghe G, Wilmer A, Hermans G, et al. (2006) Intensive insulin therapy in the medic al ICU. N Engl J Med 354: 449 \200\22361. Brunkhorst FM, Engel C, Bloos F, et al. (2008) Intensive insulin therapy and pentastarch re suscita- tion in severe sepsis. N Engl J Med 358: 125 \200\22339. See also: Hypoglycaemia, p506. This page intentionally left blank 135 Chapter 7 Wound and pressure area management Wound management principles 136 Dressing techniques 138 Special support surfaces 140 136 CHAPTER 7 Wound and pressure area management Wound management principles Wound management attempts to promote wound healing, prevent con - tamination and wound breakdown, and reduce pain and discomfort. A wound heals through the phases of haemostasis, in \202 ammation, granu- lation, and maturation. The \201 rst two processes arrest bleeding and help remove contamination. Granulation inv olves rebuilding of the tissues, angiogenesis contraction, and epithelialisation. This proc ess normally takes about 21 days, but may be delayed by age, infection, dehydration, or poo r nutrition. Maturation may take several years and involves remodeling of the dermis to inc rease the strength of the healed wound. A wound that fails to go through these process steps may become chronic. It is important to keep the wound warm and moist since all human cells (with the exception of the dead, kerat inised, super \201 cial skin cells) require moisture to survive, and warmth to grow and di vide. An exudate provides the best environment for healing by supporting cells involved in wound repair with nutrients. Although angiogenesis is increased in a low oxygen environment (e.g. under occlusive dressings), most large, randomized trials show reduction in post-ope rative wound infection from administering supplemental oxygen. Wound cleansing Wounds should be cleaned by irrigation with isotonic saline. Soaps irritate the wound but may be useful on the surrounding skin. Both iodine and peroxide irritate the wound, are unnecessary, and best avoided. Wound infection The hallmarks of wound infection are: \200 \200 \200 \200 \200 \200 \200 Pain. Redness. Increased warmth. Tenderness. Oedema. Purulent discharge. Foul odor. Systemic or spreading signs of infection (e.g. cellulitis) may be present and mandate syste mic antibiotic therapy. The wound should be swabbed prior to treatment. Otherwise, local tr eatments may be suf \201 cient, e.g. silver preparations, iodine-based preparations, and t opical antibiotic (e.g. silver sulfadiazine). The latter should only be used for short-term treatment in mild cases. Surgical debridement may occasionally be needed. Pressure sores Pressure sores occur due to compression of tissue between bone and the suppo rt surface, and due to shearing forces, friction, and maceration of tissues against the sup port surface. A pressure sore requires cleansing, debridement of eschar or necrotic tissue, staging (see table opposite), and packing if there is crater formation. Packing should occ lude the ulcer, but should be loose to avoid adding to the pressure damage. Dressings shoul d keep the ulcer moist. WOUND MANAGEMENT PRINCIPLES 137 Staging of pressure sores Stage 1 Stage 2 Stage 3 Stage 4 Skin intact with persistent redness due to pressure Ulcer involving the epidermis or dermis . Ulcer involving subcutaneous tissue layer. May be undermined. Ulcer extends through the f ascia to muscle, tendon, or bone. Undermining and tunneling may be present. Ulcer bed canno t be visualized due to slough or eschar. Unstageable Modi \201 ed from the National Pressure Ulcer Advisory Panel, February 2007. See also: Dressing techniques, p138; Special support surfaces, p140. 138 CHAPTER 7 Wound and pressure area management Dressing techniques Wound dressings serve to reduce pain, protect the wound from further in jury and infection, and reduce moisture loss. Dressings should be non- adherent, sterile, a nd cover the wound completely. Adherent dressings delay wound healing. When dressings are applied to wounds, an aseptic technique must be used. Bio-occlusive dressings These allow air and water vapor to permeate, thus accelerating heal ing; they are transparent to allow wound assessment and are waterproof. Calcium alginate Calcium exchanges with sodium from the wound to convert exudates to a gel. This reduces moisture loss. They are not effective for dry wounds since they depend on abs orption of exudates to be active. Foam dressing Foam dressings absorb excessive exudates while allowing air and vapor permeat ion to accelerate healing. They require absorption of exudates to be effective. They are th ermally insulating and non-adherent. Hydrocolloids Hydrocolloid dressings provide slow absorption of exudates to create a soft, non-adherent gel which occludes the wound and retains moisture. They are effective when exu dates are low volume. They should not be used in infected wounds as growth of anaerobes may be encouraged by their occlusive properties. Hydrogels Hydrogels have hydrophilic sites to enable absorption of excess exudates. They re tain moisture. Vacuum-assisted closure (VAC) A foam dressing is placed in the ulcer absorbing excessive ex udates. The ulcer is sealed with an adhesive drape and negative pressure is applied for up to 24h per day. The VAC dressing reduces oedema and improves local blood supply while remov ing surface debris and exudate. Intermittent treatment may be more effective than continuou s. Use of VAC dressing is advantageous in perineal pressure sores because the vacuum helps keep the dressing in place. DRESSING TECHNIQUES 139 Properties of wound dressings \200 \200 \200 \200 \200 \200 Maintain warmth. Maintain moisture. Remove exudates. Allow vapor and gas permeation. Minimi ze contamination. Non-adherent. See also: Wound management principles, p136. 140 CHAPTER 7 Wound and pressure area management Special support surfaces The use of special support surfaces attempts to reduce the pressur e at the contacting skin surface to a level below capillary occlusion pressure. In most cas es, it is suf \201 cient to use postural changes to minimize the time the support surface contacts with any one area of skin. Factors suggesting need for special support surfaces \200 Patients with severely restricted mobility due to external traction or cardiorespiratory in stability cannot be turned frequently, if at all. Patients with decreased skin integrity, e .g. burns, pressure sores already present, chronic corticosteroid use, diabetes mellitus. P atients on vasoactive drug infusions and/or poor tissue perfusion. Types of special support surface Air mattress This either replaces or is placed on top of a standard hospital bed mat- tress. Although providing minimum reduction in contact pressure , they should be considered as minimum support for patients with any of the above factors.