Anaesthetics III Flashcards
Cerebral blood flow
Cerebral blood flow (CBF) is approximately 50 ml/100 g of brain tissue per minute and is maintained at this constant rate over a wide range of mean arterial pressures (not systolic blood pressures). This phenomenon is called autoregulation and occurs between mean arterial pressures (MAP) of 60-130 mmHg.
The autoregulation curve for cerebral blood flow is shifted to the right (not left) with hypertension and is lost around areas of diseased brains.
Hypothermia is defined as a core temperature below 35°C and is associated with a reduction in CBF.
Hypercapnoea causes cerebral vasodilatation which increases CBF. In hypocapnoea the CBF falls due to cerebral vasoconstriction, for example, a reduction in PaCO2 from 5 kPa-4 kPa (40-30 mmHg) results in a 30% fall in blood flow.
CBF increases when the PaO2 falls below 6.7 kPa (50 mmHg) and is doubled at a PaO2 of 4 kPa (30 mmHg).
Cervical plexus
The cervical plexus is formed by the anterior primary rami of C1 to C4 and divides into superficial and deep branches.
The superficial branches pierce the deep fascia at the middle of the posterior border (not anterior) of the sternocleidomastoid, and provide sensation from the lower border of the mandible (not maxilla) to the level of the second rib.
The deep branches supply motor fibres to the neck muscles and diaphragm and are located in the sulci of the transverse processes.
Complications of a cervical plexus block include
• Injection of local anaesthetic into the vertebral artery, subarachnoid and epidural spaces
• Blockade of the phrenic nerve, recurrent laryngeal nerve and cervical sympathetic plexus.
Thrombosis risk
Patients with deep venous thrombosis usually present with physical signs that are unreliable or non-specific, and frequently require investigation to confirm the diagnosis. Some calf vein thromboses can be asymptomatic. Risk factors associated with DVT and pulmonary embolism (PE) include hypercoagulable states, such as deficiencies of • Protein C • Protein S • Antithrombin III • Plasminogen. Other risk factors are • Malignancy • Prolonged immobility • The oral contraceptive pill • Pregnancy • Obesity • Previous DVT • Varicose veins • Polycythaemia • Myocardial infarction • Cardiac failure • Connective tissue diseases.
Lumbar (not thoracic) epidurals and spinals have been associated with a reduced incidence of DVT. This has been attributed to the increased blood flow to the lower limbs, reduced venous stasis and reduced blood viscosity (from intravenous fluid loading).
Pulmonary embolism
A pulmonary embolus can present with
• Dyspnoea
• Pleuritic chest pain (with an audible pleural rub)
• Haemoptysis
• Cyanosis
• Pulmonary hypertension
• Right ventricular failure
• Cardiac arrest.
They can also be asymptomatic.
A pleural rub may be found on auscultation in pneumonia, so it cannot be used to confirm a PE.
A positive V/Q scan will show persistent ventilation in a region with absent perfusion (not ventilation). The presence of co-existing pulmonary pathology reduces the sensitivity of this investigation.
The associated ECG changes in a PE are not diagnostic, but include signs of right (not left) ventricular strain with right axis deviation, right bundle branch block and the S1, Q3, T3 pattern (S wave in lead I, Q wave and inverted T wave in lead III).
The classical findings on arterial blood gas analysis show
• Hypoxia
• Hypocarbia (not hypercarbia)
• An increased alveolar-arterial oxygen gradient.
Treatment of a PE requires systemic anticoagulation (heparin followed by warfarin), and in selected cases only (central PE) surgical embolectomy may be performed.
helps to prevent the development of multiple organ dysfunction syndrome (MODS) in trauma patients? Early nasogastric feeding
Multiple organ dysfunction syndrome (MODS) is defined as ‘the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention’ (1992 American College of Chest Physicians/Society of Critical Care Medicine consensus panel). It is a frequent complication of the systemic inflammatory response syndrome (SIRS) and sepsis.
Enteral feeding via a gastric tube should be started as soon as possible in all trauma patients. In the absence of enteral nutrition, the gut mucosa atrophies and bacteria may ‘translocate’, which is thought to be the cause of sepsis and MODS.
Selective decontamination of the digestive tract (SDD) may reduce the incidence of nosocomial infection, but there is little evidence to suggest it reduces the incidence of MODS. The use of broad spectrum antibiotics will merely encourage the development of resistant bacteria.
Fractures should be stabilised as soon as possible. Using propofol for long term sedation on the ICU is no longer popular; however this is not associated with the development of MODS.
Treating pain in trauma patients
Decreases muscle spasm, does not increase identification of clinical signs
Appropriate analgesia should be given to all trauma patients. Pain will usually cause immobilisation of the patient and thus increases the risk of developing venous thrombosis and venous thromboembolism.
When in pain, patients have shallow respirations and usually are reluctant to cough or sigh. This causes atelectasis and increases the risk of pulmonary infections. When adequate analgesia is provided, tidal volumes are greater with less atelectasis and a reduced incidence of pulmonary complications is seen.
Pain causes adrenergic stimulation and this increases metabolic responses, for example,
• Gluconeogenesis
• Glycolysis
• Lipolysis
• Production of free fatty acids.
Treatment of pain will decrease this response.
Pain associated with fractures can cause skeletal muscle spasm, which if left untreated not only helps to maintain the pain but can also make the reduction of fractures very difficult.
Although analgesia improves patient co-operation during examination and radiological investigation, some important clinical signs and symptoms can be masked. The interpretation of an abdominal examination may be more difficult and some cervical spine fractures have also been missed following the administration of analgesia.
Traumatic rupture of aorta
Widened mediastinum
The thoracic aorta is at risk in any patient sustaining a significant decelerating force, for example, fall from a height or high speed road traffic accident (not penetrating injuries).
Widening of the mediastinum may have been overlooked on the original AP radiograph. This is a sensitive sign of aortic rupture, though not very specific: 90% of widened mediastina are due to venous bleeding.
Other features frequently associated with aortic rupture are:
• Fractures of the upper three ribs
• Deviation of the trachea to the right
• Depression of the left mainstem bronchus
• Deviation of the nasogastric tube to the right
• Loss of the aortic knob
• Pleural capping.
Interscalene block Can cause ipsilateral horners syndrome
An interscalene block anaesthetises the brachial plexus at the level of the roots, and reliably blocks the shoulder and radial aspect of the forearm. It is often associated with sparing in the ulnar nerve territory (not radial).
The key landmark for performing this block is the interscalene groove which is located between the anterior and middle scalenus muscles. At least half of patients having an interscalene block develop Horner’s syndrome on the same side (ipsilateral).
One of the main advantages of the interscalene block is that pneumothorax is avoided, and the supraclavicular block is associated with the highest risk of pneumothorax.
Nerves to be blocked in an ankle block
In order to perform an ankle block, five nerves need to be anaesthetised.
They are the saphenous nerve (the terminal branch of the femoral nerve) and four nerves derived from the sciatic nerve:
• Tibial nerve
• Sural nerve
• Superficial peroneal nerve
• Deep peroneal nerve (not common peroneal nerve).
Muscle of inspiration
Scalenus anterior
The internal intercostals are muscles of expiration.
Latissimus dorsi has no role in either inspiration or expiration.
The rectus abdominus aids expiration by pushing the relaxing diaphragm upwards and pulling the ribs down and in.
In deep forced inspiration, every muscle that can raise the ribs is brought into action, including the scalenus anterior and medius and the sternocleidomastoid muscle.
Femoral nerve
Supplies part of foot but not in femoral sheath, and doesn’t share origin with sciatic nerve
The femoral sheath contains the femoral artery and vein as well as lymphatics, but not the nerve. The femoral nerve lies behind and lateral to the sheath.
The femoral nerve gives off three cutaneous branches
• Two from its anterior division (medial and intermediate cutaneous nerves of thigh which supply the skin of the medial and anterior surfaces of the thigh)
• One from its posterior division (saphenous nerve).
It has no branches to the scrotum.
The saphenous nerve runs down the medial side of the leg and supplies the medial side of the calf as far as the medial malleolus. It terminates in the region of the ball of the big toe and may supply the medial side of the dorsum of the foot.
The femoral nerve is the largest branch of the lumbar plexus and comes from the same lumbar nerves as the obturator nerve, L2, L3 and L4.
Hyperkalaemia treatment
When electrocardiogram abnormalities are present, treatment of hyperkalaemia is an emergency. The treatment includes
• Calcium chloride
• Sodium bicarbonate
• Dextrose/insulin
• Beta agonists
• Loop diuretics
• Drugs to bind potassium in the gastro-intestinal tract
• Dialysis.
The underlying condition must also be sought and treated.
Amiloride, atenolol, magnesium and phosphate have no role in the management of hyperkalaemia.
Causes of hypokalaemia
Causes of hypokalaemia can be divided into the following: • Transcellular shifts o Alkalosis o Insulin o Beta-agonists • Renal losses o Diuresis o Diabetic ketoacidosis after therapy o Conn's disease • Extrarenal losses o Diarrhoea o Nasogastric suction • Decreased intake o Malnutrition o Alcoholism. Angiotensin converting enzyme inhibitors and rhabdomyolysis tend to cause hyperkalaemia.
Regarding burns
Full thickness are painless
Chemical burns should be brushed off (if dry substance) and irrigated. Using an alkaline substance to neutralise the acid may result in an exothermic reaction (generating heat), which could exacerbate the injury.
Superficial partial thickness burns are painful and erythematous, deep partial thickness burns are blistered and very painful, and full thickness burns are white, leathery and painless.
The anterior trunk is 13% of body surface area (Lund and Browder chart). The ‘rule of nines’ is just a simple approximation.
The half-life of carboxyhaemoglobin in 100% oxygen is approximately 30 minutes; in air it is four hours.
Principles of traumatic head injury
Principles in the management of a head injury include
• Nursing the patient in a head up tilt of 30 degrees (not down)
• Avoiding hypoglycaemia and hyperglycaemia
• Using normal saline (0.9%) as the primary maintenance fluid
• Maintaining normocapnoea (not hyperventilation to a pCO2 of 3.0 kPa)
• Active treatment of fever and seizures.
The prophylactic treatment of seizures has not shown to be of benefit.
Severe traumatic brain injury Loss of autoregulation
Primary brain injury is usually irreversible and occurs at the time of injury.
Causes of secondary brain injury include
• Hypoperfusion
• Hypoxia
• Reperfusion injury.
The factors that determine the cerebral perfusion pressure (CPP) include the mean arterial blood pressure (not systolic blood pressure) and the intracranial pressure (ICP) as shown in the following equation:
Cerebral perfusion pressure = mean arterial pressure - intracranial pressure.
The cerebral perfusion pressure is usually maintained above 70 mmHg.
In severe traumatic brain injury, the autoregulation of cerebral blood flow is lost.
Cerebral oxygen consumption should be minimised following head injury (not maximised).
GCS
The Glasgow coma score (GCS) provides a score from 3 to 15, depending on the best response observed in three different parameters. The minimum score is 1 in each of these.
• Eye opening
• Verbal response
• Motor response.
The pupil response to light is not included.
The GCS was originally developed for use in brain trauma but is now used when evaluating other cerebral insults.
A modified version is used in young children.
Hypovolaemic shock
CVP pressure is reduced
False:
Hypovolaemic shock occurs when the intravascular volume is depleted as a consequence of blood or fluid loss.
The commonly encountered haemodynamic findings include
• A decrease in stroke volume, cardiac output and filling pressures (that is, central venous pressure and pulmonary capillary wedge pressure)
• An increase in heart rate and systemic vascular resistance.
Invasive arterial measurement complication
False aneurysms Complications of arterial cannulation include • Haematoma formation • Distal ischaemia • Infection • Embolisation • False aneurysm • Arteriovenous fistula • Blood loss. Flush volumes must be limited in children, otherwise fluid overload may occur. Replacing the pressure bag with a syringe pump may provide some protection against such an occurrence.
Inappropriate cannulation site
Brachial artery
Commonly used sites for the insertion of arterial cannulae include the radial, femoral, axillary and dorsalis pedis arteries.
Short catheters should be used for the radial and dorsalis pedis arteries.
Longer, softer and more flexible cannulae should be used for the femoral and axillary arteries (to minimise injury).
The brachial artery should be avoided because the collateral circulation is limited.
ARDS
ARDS is diagnosed when all the following are present
• Acute onset of impaired oxygenation
• Severe hypoxia where the paO2:FiO2 ratio is
Life threatening asthma features
Asthma may be classified as 1. Moderate exacerbation 2. Acute severe 3. Life-threatening 4. Near fatal. The features of life-threatening asthma are • A peak expiratory flow rate (PEFR)
Metabolic acidosis causes
The causes of a metabolic acidosis include
• Renal failure
• Gastrointestinal bicarbonate loss
• Drug poisoning (for example, salicylates, diabetes mellitus, starvation and lactic acidosis).
The other options all cause a metabolic alkalosis (hyponatraemia/kalaemia, calcium antacids, hypochloraemia)
Increased pulmonary capillary wedge pressure
Fluid overload and left ventricular failure (LVF) cause an increase in pulmonary capillary wedge pressure (PCWP).
The PCWP may misrepresent the left ventricular end-diastolic pressure (LVEDP) in
• Pulmonary venous obstruction (pulmonary fibrosis, vasculitis, atrial myxoma)
• Valvular heart disease (mitral stenosis, mitral regurgitation and aortic regurgitation).
Steroid use
Not in LVF Yes in: ARDS Asthma Sepsis Meningitis Steroids decrease the incidence of deafness following Haemophilus influenzae type B (Hib) meningitis. They are used as a first line treatment in asthma. Steroids are in the guidelines for the management of sepsis, and decrease the incidence of fibrosis if given at 10-14 days in ARDS.
Use of tourniquets
Tourniquets may be used in the elderly and in diabetics who do not have peripheral neuropathy.
They are contraindicated in patients with sickle cell disease, any peripheral vascular disease (including deep vein thrombosis) and limb infections.
APACHE II scoring system
The APACHE II score is a form of physiological scoring system which devises a score by taking the following three factors into consideration:
1. Acute physiological score
2. Age of the patient
3. Previous health condition.
The acute physiological score takes into account the following factors:
• Rectal temperature (°C)
• Mean blood pressure
• Heart rate
• Respiratory rate
• Alveolar-arterial oxygen gradient if FiO2 >0.5, or PaO2 if FiO2 75 years with 75 scoring ‘6’ points.
One of the factors in previous health condition (chronic health points) includes immunocompromised status. There are also scores for
• Post-operative admission
• Non-operative admission
• Emergency operation.
Higher APACHE II score is associated with a higher risk of hospital death.
Complications of laparoscopic surgery
Endobronchial intubation may result from cephalad displacement of the trachea during high pressure peritoneal insufflation. The position of the endotracheal tube should always be checked intra-operatively once gas insufflation has commenced.
Aspiration of gastric contents may occur from
• Increased intra-abdominal pressure
• Changes in position
• Gastric manipulation.
A tension and simple pneumothorax may be caused by
• Gas tracking along tissue planes
• Pulmonary barotrauma
• Undiagnosed diaphragmatic hernia
• Damaged pleura
• Ruptured bulla.
Venous gas embolism, which is extremely rare, is usually caused by accidental intravascular injection of gas into a vein. It may also, very rarely, arise from the tip of a cooled laser.
Effective preoperative anti-emetic
Ondansetron
Atropine, an anticholinergic, is seldom used for its anti-emetic effects which are weak, as it causes tachycardia and is preferentially used to dry up secretions.
Midazolam and lorazepam are benzodiazepines and are anxiolytics.
Metoclopramide is used pre-operatively to stimulate gastrointestinal emptying, but is rather ineffective due to short duration of action as a pre-operative anti-emetic in standard doses (10 mg).
Ondansetron is an effective anti-emetic.
Sickle cell pt with ?appendicitis
The initial management of the patient with abdominal pain, whether it is due to appendicitis or a sickle crisis, is to provide oxygen, intravenous opioid analgesia and fluids.
Sickle cell anaemia is a haemoglobinopathy caused by substitution of valine for glutamic acid at position 6 (from the N-terminal) of the beta chain. Homozygotes contain only abnormal haemoglobin (HbSS) which depolymerises at a PO2 of 5-6 kPa, which is found in normal venous blood. Thus, sickle cell disease (HbSS) patients are continuously sickling.
Heterozygotes contain both normal and abnormal haemoglobins (HbAS) and are said to have sickle cell trait. These patients only sickle at extremely low PO2 values of 2.5-4 kPa.
Sickle cell crises are caused by acute vascular occlusion, which is associated with severe pain, which can mimic an acute abdomen. In addition to hypoxaemia, sickling can be precipitated by
• Hypothermia
• Dehydration
• Infection
• Exertion
• Stress.
Thus the peri-operative management of sickle cell disease patients involves keeping them well oxygenated, warm, well hydrated, providing adequate analgesia by PCA (patient controlled analgesia) and avoiding acidosis (venous stasis).
Exchange blood transfusions may be required by HbSS patients before major elective surgery, the aim being to lower the HbS concentration to 30-40%, which would be impossible to organise before emergency surgery.
Haemoglobin electrophoresis is the only investigation which can determine the nature of the haemoglobinopathy, but is rarely performed out of hours.
A Sickledex test will detect HbS but provides no information on other haemoglobins.
An FBC will usually show a low haemoglobin in sickle cell disease, but it can be normal in sickle cell trait and a blood film will show sickle cells.
Pancreatitis
Acute pancreatitis is an autodigestive process which is commonly associated with biliary tract disease or excessive alcohol intake. Other recognised causes include • Abdominal trauma • Mumps • Hypothermia • Diuretic • Steroid therapy. The classical laboratory findings include • A raised serum amylase • Leucocytosis • Hyperglycaemia • Hypocalcaemia • Hypoproteinaemia • Hyperlipidaemia. An abdominal x ray may reveal a 'sentinel loop' of small bowel overlying the pancreas. The chest x ray can show a wide range of pathology. Poor prognosis may be indicated by: • Age >55 years • Systolic blood pressure 15 x 109/l • Temperature >39°C • Glucose >10 mmol/l • PaO2 15 mmol/l • Calcium
PA CXR
Rotation of the patient causes the lungs to have a difference in translucency
The PA chest x ray is performed in the radiology department and is a high quality radiograph which differs from the portable anteroposterior (AP) chest x ray which is of inferior quality.
The technique of taking a PA chest x ray involves a patient standing with their back to the x ray source, with the anterior chest wall against the film plate. It should ideally be taken at full inspiration, otherwise the appearance of abnormal lung base shadowing and cardiac enlargement may be seen.
When the x ray penetration is sufficient the thoracic vertebrae can be visualised on the radiograph, which ensures that the pulmonary vessels behind the heart are well seen. In an adequately centred x ray the medial ends of the clavicles should be equidistant from the spinous processes in the midline of the thoracic spine. If the patient is rotated then it can cause the lungs to have a difference in translucency, which can mimic pulmonary disease. The hilum and heart may also look enlarged.
Normally the right hemidiaphragm is higher than the left by 1.5-2 cm and a difference of more than 3 cm may be significant. In hyperinflation they may be at the same level and when the stomach or splenic flexure is distended the left hemidiaphragm may be higher than the right.
As a normal variant, bowel may be interposed between the liver and the right hemidiaphragm; this is known as Chilaiditi’s syndrome.
Horners syndrome
Horner’s syndrome results from interruption of the sympathetic innervation to the head. It was originally described with cervical lesions causing damage to the T1 contribution to the cervical sympathetic chain, but may be due to lesions anywhere along the sympathetic pathway.
The features of Horner’s include
• Partial ptosis
• Myosis (contraction)
• Apparent enophthalmos
• Lack of sweating
• Nasal stuffiness on the affected side.
Myosis occurs due to paralysis of the dilator pupillae and ptosis is due to paralysis of the sympathetic muscle fibres transmitted via the oculomotor nerve to the upper eyelid.
Horner’s may follow
• Operations on, or injuries to, the neck in which the cervical sympathetic chain is damaged
• Malignant invasion from lymph nodes or adjacent tumour
• Spinal cord lesions at the T1 segment.
Lap chole for a rh arthritis patient
Rheumatoid arthritis is a systemic connective tissue disease which presents as a symmetrical arthropathy involving any joint (except the terminal interphalangeal joints).
Lung involvement usually causes fibrosis and hence a restrictive pattern on lung function testing.
Atlanto-axial ligament laxity, together with odontoid peg erosion, may result in cervical subluxation and possible cord compression.
Twenty five per cent of rheumatoid arthritis sufferers have cervical instability, but only 7% have clinical signs. Cervical spine x rays are required and a gap of more than 3 mm between the odontoid peg and the posterior arch of the axis is diagnostic of subluxation.
Cricoarytenoid involvement may cause hoarseness, stridor and airway obstruction. A normochromic normocytic anaemia plus anaemia from chronic gastrointestinal loss (NSAIDs) are often found on a pre-operative FBC.
Bone marrow suppression is a side effect of gold therapy and penicillamine can cause thrombocytopenia.
Pancytopenia associated with hepatosplenomegaly is termed Felty’s syndrome.
A 20-year-old male has sustained 15% burns in a house fire.
Colloid is the principal agent used for fluid resuscitation in the Mount Vernon formula
The rule of 9s is used to approximate the body surface area (BSA) burnt. Adults • Head: 9% • Upper limbs: 9% each • Lower limbs: 18% each • Trunk: 18% front and 18% back • Perineum: 1%. Adults can compensate with oral fluids for up to a 15% burn but children can only compensate for a burn
A 65-year-old male is two days post-operation following an elective repair of an abdominal aortic aneurysm. Surgery was uncomplicated and the aortic cross clamp time was below average.
He has a low dose epidural infusion for analgesia. The patient complains that he feels paralysed below his waist.
Ischaemic damage to the spinal cord occurred during aortic cross clamping
The main differential diagnosis in this scenario is whether his symptoms are
• Related to the epidural
• A consequence of aortic cross clamping.
Low dose epidural infusions are weak concentrations of local anaesthetic agents delivered by a syringe pump. They are popular because they block sensory fibres but spare motor function, thus could not be totally responsible for his symptoms.
Direct spinal cord injury from the epidural Tuohy needle is rare. The risk can theoretically be further reduced if the epidural technique is performed on patients who are awake using local anaesthesia.
Epidural haematoma formation with spinal cord compression is extremely rare with normal coagulation. The presence of such a haematoma is unlikely to be masked by low dose local anaesthetic infusions in the epidural space. Permanent neurological damage may occur if surgical decompression is delayed.
Epidurals can also be safely inserted into patients scheduled for anticoagulation, but are contraindicated in patients who are already anticoagulated.
The spinal cord is supplied by an anterior spinal artery, two posterior spinal arteries and several radicular branches that feed the spinal arteries. The most important radicular branches are located at T1 and at the lower thoracic/upper lumbar levels. The latter is called the artery of Adamkiewicz.
Cord ischaemia can occur, but anterior spinal artery syndrome usually only occurs with severe hypotension, and since surgery was uncomplicated this option is unlikely. The actual location where the artery of Adamkiewicz supplies the spinal arteries is not known. Therefore, aortic cross clamping exposes patients to the potential risk of distal spinal cord ischaemia even when the cross clamp time is short.
Secondary damage to the cord can also occur during reperfusion.
Ischaemic damage to the spinal cord occurred during aortic cross clamping
The main differential diagnosis in this scenario is whether his symptoms are
• Related to the epidural
• A consequence of aortic cross clamping.
Low dose epidural infusions are weak concentrations of local anaesthetic agents delivered by a syringe pump. They are popular because they block sensory fibres but spare motor function, thus could not be totally responsible for his symptoms.
Direct spinal cord injury from the epidural Tuohy needle is rare. The risk can theoretically be further reduced if the epidural technique is performed on patients who are awake using local anaesthesia.
Epidural haematoma formation with spinal cord compression is extremely rare with normal coagulation. The presence of such a haematoma is unlikely to be masked by low dose local anaesthetic infusions in the epidural space. Permanent neurological damage may occur if surgical decompression is delayed.
Epidurals can also be safely inserted into patients scheduled for anticoagulation, but are contraindicated in patients who are already anticoagulated.
The spinal cord is supplied by an anterior spinal artery, two posterior spinal arteries and several radicular branches that feed the spinal arteries. The most important radicular branches are located at T1 and at the lower thoracic/upper lumbar levels. The latter is called the artery of Adamkiewicz.
Cord ischaemia can occur, but anterior spinal artery syndrome usually only occurs with severe hypotension, and since surgery was uncomplicated this option is unlikely. The actual location where the artery of Adamkiewicz supplies the spinal arteries is not known. Therefore, aortic cross clamping exposes patients to the potential risk of distal spinal cord ischaemia even when the cross clamp time is short.
Secondary damage to the cord can also occur during reperfusion.
Postoperative ileus
Can occur after most abdo ops
Intestinal atony occurs to some extent after most abdominal operations. However, even in the presence of this post-operative ileus, small bowel activity can continue despite gastric and colonic stasis.
The aetiology is thought to include
• Intra-operative bowel manipulation
• Sympathetic overactivity
• Peritoneal irritation (for example, from blood)
• Electrolyte imbalances, especially hypokalaemia.
The presence of increased bowel sounds and colicky abdominal pain suggest mechanical obstruction, which can follow an ileus.
The ileus usually resolves within 48 hours, although the presence of bowel sounds is not a reliable indicator.
Hypokalaemia
Hypokalaemia is defined as a serum potassium of less than 3.5 mmol/l, and symptoms usually occur below 2.5 mmol/l.
A common cause of post-operative hypokalaemia is inadequate potassium intake, for example, intravenous fluid therapy without sufficient potassium supplementation. The daily maintenance potassium requirement is 0.5-1.0 mmol/kg per day.
ECG changes are common and include
• T wave inversion
• S-T segment depression
• Q-T and P-R prolongation
• U waves.
Cardiac arrest may occur if attempts to raise the serum potassium are delayed and hypokalaemia is a cause of pulseless electrical activity (PEA).
Treatment of hypokalaemia in this patient should be with intravenous potassium, as he may still be on restricted oral intake or even be nil by mouth. Up to 40 mmol of potassium chloride can be added to each litre bag of fluid, but this method may not raise the serum potassium quickly enough. Therefore, it should be given by intravenous infusion at a rate not exceeding 40 mmol/hour.
In severe cases this upper limit may be exceeded with ECG monitoring, for example, in critical care areas, as there is a high risk of dysrhythmias, especially ventricular fibrillation.
