ANSWER TO SELF - ASSESSMENT

Pre-operative Management

Intra-operative and postoperative management

Pre-operative Management

Although this patient has already undergone a number of special investigations and been in hospital a number of hours it is unfortunate that he has not yet received any treatment. Much of the initial resuscitation and treatment that he requires can occur without a specific diagnosis, and the sooner it is started the better. It may be useful to consider an A, B, C approach to his initial management.

Airway assessment: Conscious and maintaining his own airway. Start facemask oxygen. This patient has acute on chronic respiratory compromise, signs of poor perfusion and a low haemoglobin concentration (see Circulation) which will all result in a decreased oxygen delivery. His oxygen consumption is also likely to be raised due to the local and systemic effects of the bowel obstruction. Facemask oxygen will increase his arterial PO₂ and go some way to improving his oxygen delivery.

Oxygen delivery (mls O₂/min) = Hb (g/l) x 1.31 (mlsO₂/g Hb) x arterial O₂ saturation/100 x cardiac output (l/min). (See Update 10 for a full explanation)

Breathing assessment: The patient is hypoxic due to venous admixture. The cause is pulmonary shunt and V/Q mismatch secondary to chronic lung disease, and pulmonary atelectasis caused by abdominal distension and diaphragmatic splinting. The respiratory drive is increased and the arterial blood gas shows a partially compensated metabolic acidosis. Management: Facemask oxygen and NG tube to decompress the bowel. There are a number of potential causes for the metabolic acidosis. (base excess of -8). Anaerobic metabolism with lactic acid production secondary to a global reduction in oxygen delivery (shock), anaerobic metabolism in ischaemic bowel, acidosis due to decreased renal perfusion (shock) and loss of bicarbonate into the gut (balanced to some extent by a loss of acidic gastric secretions). Chemoreceptors in the carotid bodies sense the decrease in pH and respond by increasing ventilation. This results in a fall in pCO₂ and a respiratory alkalosis. Ventilation will also be increased in response to a low pO₂ stimulating the aortic and carotid bodies, however pO₂ values less than 8 kPa are necessary to produce the maximum response. Remember that the receptors that are normally the most important for the control of ventilation are those situated in the medulla. These respond to a high CO₂ level in the blood because of the effect that this has on reducing the cerebrospinal fluid pH. The Henderson-Hasselbach equation describes how the pH of the blood is due to a combination of respiratory and metabolic components. Tight control of pH is vital for metabolic processes and therefore the respiratory alkalosis (low CO₂) in this case is a physiological response designed to counteract the effect on pH of a metabolic acidosis (low HCO₃).

Circulation assessment: Dehydration (based on the history you know the patient will be dehydrated but this is confirmed by the dry mouth and the urea/creatinine ratio). Additional signs might include decreased skin turgor, sunken eyes, absence of sweating and decreased urine output. Poor perfusion/shock - increased heart rate, low BP, cold peripheries and acidosis. This is caused by fluid loss into the bowel and peritoneum, and losses due to vomiting. Septic shock due to bacterial translocation across the gut wall or due to local complications such as perforation or strangulation may also be the cause. Anaemia (the haemoglobin will be lower than this when rehydrated). Probably due to chronic blood loss into the gut and an 'anaemia of chronic disorders'.

Correct the intravascular deficit immediately. Remain with the patient and assess the response to repeated fluid boluses. In this patient a colloid should be used initially but blood should be used when it is available. Send blood for cross-match (4 units) and coagulation tests. A decrease in heart rate, increase in blood pressure and improvement in peripheral perfusion are the changes that one would hope to see at the bedside.

Insert a urinary catheter and monitor the urine output.

Correct dehydration. Intravenous crystalloid should be prescribed to replace lost water and electrolytes. (see explanation below).

Consider inserting a CVP line. Useful to guide fluid therapy especially in the elderly and those with impaired cardiac function and to give inotropes if necessary. There is no need for this to be inserted immediately. It may also be useful to aspirate mixed venous blood and determine its oxygen saturation. Patients with a mixed venous oxygen saturation of less than 70% have a high global oxygen extraction due to a low oxygen delivery compared to oxygen consumption. They may benefit from attempts to increase oxygen delivery with further fluids and inotropes. An acidosis that persists in patients with a high mixed venous oxygen saturation (implying an adequate oxygen delivery) may be due to renal failure or ischaemic bowel. It is also sometimes seen in the late stages of septic shock and is thought to be due to microcirculatory abnormalities or 'sick' cells that are unable to utilise the oxygen supplied to them.

Inotropes as necessary.

The fluid and electrolyte abnormalities that occur in bowel obstruction depend on the site of the obstruction. It is important to understand how the various biochemical abnormalities arise and how to treat them. Pyloric obstruction causes a loss of H⁺ and Cl^- (and Na⁺ and K⁺) due to vomiting acidic gastric secretions. Alkaline pancreatic and duodenal secretions are retained and the result is a hypochloraemic metabolic alkalosis. This affects the renal handling of Na⁺. Na⁺ is normally reabsorbed in the proximal tubule for which Cl^- needs to be available, as HCO^3-, the only other significant anion, cannot pass easily through the proximal tubular cell wall. Initially HCO₃-, and Na+ are lost in the urine. Subsequently an increase in aldosterone caused by a reduction in circulating plasma volume causes Na+ to be reabsorbed distally in the tubule in exchange for K+ and H+ making the alkalosis worse and causing hypokalemia. The result is a hyponatremic, hypokalemic, hypochloremic metabolic alkalosis.

Mid or high small bowel obstruction presents a different picture. Large volumes of fluid are lost (Na+, K+ and water) as the absorption of saliva, bile, gastric, pancreatic and duodenal secretions are impaired (the gastrointestinal tract secretes 8 litres of fluid a day). The loss of a combination of alkaline intestinal secretions and acidic gastric secretions prevents the development of a metabolic alkalosis.

In low small bowel obstruction and large bowel obstruction fluid loss tends to be less initially as much of the water and solute secreted into the gut can be absorbed above the obstruction. In all the above situations if the obstruction is not relieved and intravenous fluid replacement does not take place the combined effects of decreased fluid intake, vomiting, fluid loss into the bowel and peritoneum, bowel perforation, bowel ischaemia, peritonitis and sepsis leads to circulatory collapse and metabolic acidosis.

In all cases of dehydration due to bowel obstruction there is a total body deficit of Na+ and water and therefore whatever the Na+ concentration (i.e. whether the patient is hyponatremic or hypernatremic) replacement needs to be with a fluid with a high Na+ content (0.9% saline or Hartmanns solution). K+ should be added to the fluid as necessary (usually 20-40mmol/l provided the patient is not anuric or hyperkalaemic). The aim should be to correct the dehydration over 24 hours, giving half the calculated amount in the first 8 hours and the second half over the following 16 hours. If the patient is very hypernatremic (Na+ > 155mmol/ l) rehydration should be over 48 hours because of the risk of

cerebral oedema. It is often helpful to crudely classify the extent of dehydration as 5%, 10% or 15% rather than as mild, moderate or severe because this enables one to estimate roughly what the fluid deficit might be. A patient that is 5% dehydrated has lost 50 ml/kg of fluid and a patient that 10% dehydrated has lost 100ml/kg of fluid etc. This calculation serves as a useful starting point when prescribing rehydration fluid but it needs to be emphasised that the rate of fluid administration should be increased or decreased depending on the results of future assessments.

Returning to the example above, the patient will need intravenous fluids to be administered to take account of the following:

• Maintenance fluid - 2000 - 3000mls/day
• Ongoing losses. Initially difficult to quantify but includes NG loss and loss into bowel. A conservative estimate would be 2000 mls/day
• Fluid deficit - If 7.5% dehydrated then the deficit is 75mls/kg or 5250mls
• Therefore the total fluid requirement for the first day is about 10 litres. Rehydration should therefore be started with 0.9% saline + 20mmol/l KCl at 600mls/hour for the first 8 hours. Frequent reassessment will be necessary and the rate of fluid administration adjusted accordingly.

Once the above treatment has been commenced the surgeon and anaesthetist should decide together when they think that the patient will be in an optimum condition to undergo an operation. Ideally the patient would go to theatre when fully rehydrated but surgical urgency may dictate otherwise. The natural history of bowel obstruction is that the bowel above the obstruction initially increases its blood supply and peristalsis in an attempt to overcome the obstruction. If the obstruction is not relieved the bowel dilates and then becomes flaccid. The distension is caused by gas (nitrogen and hydrogen sulphide) due to bacterial overgrowth and unabsorbed digestive juices. The intramural vessels become stretched and the bowel wall becomes oedematous and ischaemic. Eventually fluid leaks out into the peritoneum and perforation or necrosis of the bowel wall may occur. Patients with necrosed or perforated bowel will need to proceed to operation as early as possible and it may not be possible to rehydrate them fully before operation. A very high WCC (>25 x10⁹/l) or peritonitis may signify these complications and the localised tenderness in this may also increase the surgical urgency. A reasonable compromise in this case may be to plan to do the laparotomy after 8 hours of resuscitation when hopefully the shock and anaemia will have been corrected and the patient will have received about 5000mls of rehydration fluid. Other factors that should be considered are the need for thromboembolism prophylaxis and antibiotics.

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Intra-operative and postoperative management

After adequate preparation and monitoring the NG tube should be aspirated and anaesthesia should be induced using a rapid sequence induction technique with cricoid pressure. Large bore venous access should be obtained if this is not already in place. A CVP line will be useful to guide intra-operative fluid therapy and an arterial line will allow beat-by-beat assessment of blood pressure and facilitate the intraoperative monitoring of haemoglobin concentration, acid-base balance and electrolyte concentrations. If the patient's coagulation status is normal an epidural may help provide high quality postoperative pain control, and will decrease the likelihood of postoperative pulmonary morbidity. It may be prudent not to use the epidural immediately, but rather to establish the block cautiously during the operation. The use of epidural anaesthesia combined with general anaesthesia in a partially rehydrated, elderly patient having emergency surgery with the potential to develop a systemic inflammatory response and intra-operative fluid shifts may cause profound hypotension, and therefore caution is essential. Intra- operative hypothermia should be prevented by the use of fluid warmers and a warming mattress.

Intra-operative fluid requirements include the pre-operative requirements and in addition replacement of blood loss and 'third space' losses. 'Third space' loss is the loss of extracellular fluid that occurs during a laparotomy due to the trauma, manipulation and retraction of the abdominal contents. It is not possible to measure this but it usually amounts to about 10mls/kg/hour of surgery of this magnitude.

Measurement of pulse rate, CVP and urine output will help to guide fluid therapy intra-operatively. An oesophageal doppler monitor provides an additional non-invasive measure of cardiovascular output and filling in some centres. At the end of the procedure a decision will need to be made as to whether it is appropriate to wake the patient up and extubate him. Patients who are hypothermic, cardiovascularly unstable or very acidotic should be ventilated postoperatively, and managed on an intensive care unit.

If this patient is extubated, good analgesia will enable him to cough and breath deeply, and chest physiotherapy will help to prevent pulmonary atelectasis and infection. NSAIDs should be used with caution because of their propensity to precipitate acute tubular necrosis in elderly, dehydrated patients. Nutritional support is very important in this patient because of the period without adequate nutritional intake pre-operatively and because of the catabolic effect of cancer and surgical trauma. NG feeding should be started as soon as the surgical procedure allows. Postoperative oxygen, fluids, DVT prophylaxis and antibiotics should be prescribed as indicated. A bed on the High Dependency Unit, if available, is the most appropriate place to care for this patient.

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