Postoperative and obstetric patients

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CHAPTER 14 POSTOPERATIVE AND OBSTETRIC PATIENTS

PERI-OPERATIVE OPTIMIZATION

There is ongoing interest in so-called ‘peri-operative optimization’ of cardiovascular variables in order to minimize the physiological disturbances and stress responses caused by surgery. In some centres, patients may be admitted to ICU or HDU preoperatively, invasive haemodynamic monitoring instituted, and fluids and inotropes used judiciously to optimize stroke volume. The process is similar to that described previously in Chapter 4. (See Optimization of cardiovascular system, p. 78.) There is some evidence that peri-operative optimization reduces peri-operative complications and reduces the need for unplanned ICU admission (or length of ICU stay) after major surgery.

This is a complex area. Some patients with ischaemic heart disease, for example, may benefit from β-blockade to protect the myocardium, rather than being driven with inotropes. Seek advice and follow local protocols.

STRESS RESPONSE TO SURGERY AND CRITICAL ILLNESS

The local and systemic inflammatory responses to tissue injury and illness vary between patients, and may vary from mild pyrexia to systemic inflammatory response syndrome (SIRS), multiple organ failure and death. The clinical magnitude of this response depends in part on the extent of the injury, although other factors, including infection, immune status, genetic predisposition and physiological reserve, are also important. In addition to these inflammatory responses, which are mediated by cytokines, there are a number of physiological hormonal and metabolic responses to injury and critical illness, which are collectively known as the stress response. (See SIRS, p. 326.)

Hormonal responses

The secretion of the pituitary hormones antidiuretic hormone (ADH), adrenocorticotrophin (ACTH) and growth hormone (GH) is increased. ADH causes salt and water retention and also has vasopressor activity. ACTH leads to increased secretion of adrenal corticosteroids, cortisol and aldosterone, which further lead to salt and water retention. Growth hormone has a hyperglycaemic effect, but this effect is variable.

There is a generalized increase in sympathetic activity and the adrenal secretion of catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine) is increased. These have predictable cardiovascular effects. Adrenaline also has metabolic effects, most notably hyperglycaemia. Increased production of renin from the kidney leads to activation of the renin–angiotensin–aldosterone pathway. Angiotensin II is a potent vasoconstrictor that increases blood pressure, while aldosterone increases renal salt and water retention.

Metabolic effects

The primary metabolic effects of the stress response are those of salt and water retention and increased catabolism. Salt and water retention is multifactorial in origin. The degree of water retention may exceed that of sodium retention, such that hyponatraemia is common.

The catabolic effects of catecholamines, steroids and growth hormone include increased glycogenolysis and gluconeogenesis, resulting in hyperglycaemia. Endogenous insulin production is increased in response, but an insulin infusion is often required to control the blood sugar. Fat and protein are broken down to provide energy substrates for tissue repair.

Role of the stress response

The stress response has evolved to provide survival advantages following severe injury or during critical illness. There is evidence that those that fail to mount an appropriate physiological response to critical illness have a poor outcome despite maximal support (e.g. elderly patients following trauma, burns or apparently minor head injury). At times, however, the stress responses can be detrimental. For example, exaggerated cardiovascular responses can lead to myocardial ischaemia and impaired tissue perfusion. Increased salt and water retention can lead to oliguria. Extreme catabolic responses can lead to severe wasting. For these reasons, there has been a great deal of interest in attempting to reduce the stress response.

The most important factors in reducing the stress response are ensuring good quality anaesthesia and peri-operative care, where possible preventing or minimizing tissue injury (e.g. laparoscopic surgery), careful fluid resuscitation, and good postoperative pain relief. (See Postoperative analgesia below.)

POSTOPERATIVE ANALGESIA

Patient-controlled analgesia (PCAS)

These techniques are extensively used to provide analgesia particularly in postoperative patients. Typically the patient will be established on such a device prior to transfer to a general ward. Although not intended for operation by nurses, they have been used safely and conveniently in this way in an ICU setting.

Care should be taken in setting devices up; a dedicated intravenous catheter or non-return valve should be used. There have been a number of problems due to excessive background dosing, surges of morphine on unblocking i.v. lines, and siphoning of contents under gravity from syringes. Avoid background infusions if possible. Position syringe drivers below the level of the patient to avoid siphoning, and use antireflux valves on giving sets. A typical PCAS regimen is shown in Box 14.1.

Box 14.1 Typical PCAS regimen

50 mg morphine in 50 mL 0.9% saline

5-min lockout time

No background infusion

Regional blockade

An increasing number of patients undergoing major surgery have analgesia provided by the epidural and spinal route. These techniques may also be used to relieve pain from trauma (e.g. fractured ribs) and ischaemic limbs.

Potential advantages include the avoidance of centrally acting sedative analgesic drugs, resulting in a more awake, cooperative and pain-free patient, who is better able to cough and clear airway secretions. In addition, in patients with ischaemic limbs, neuroaxial blockade (which includes sympathetic blockade) may provide both analgesia and improvement in perfusion of the ischaemic limb.

Detailed description of epidural techniques is beyond the scope of this book. When a patient is admitted with an epidural catheter in situ, you should make sure that you confirm the analgesic regimen with the responsible anaesthetist. Local anaesthetic and opioid drugs may be used alone or in combination. If opioid drugs are administered, additional systemic opioids should be administered with care because of the risk of respiratory depression. Typical regimens are shown in Table 14.1.

TABLE 14.1 Typical postoperative epidural infusion regimens

Agent	Rate	Comment
Bupivicaine 0.1–0.15%	8–15 mL / h
Bupivicaine 0.1–0.15%plus fentanyl 2 μg / mL	8–15 mL / h	No concomitant systemicopioids to be given

If breakthrough pain occurs and the patient is otherwise stable, give a 5–10 mL bolus of the epidural solution and then increase the infusion rate. This is normally effective within 10–15 min. Beware of hypotension.

Do not prescribe or administer epidural drugs if you are not familiar with epidural techniques. Seek help.

Complications of epidural blockade

The potential complications of epidural blockade are shown in Box 14.2.

Hypotension usually responds to fluid loading (500 mL colloid) and reducing the rate of epidural infusion. If significant hypotension develops, reduce or stop infusion and consider the use of a vasopressor infusion.

Significant muscle weakness can usually be avoided by the use of low concentrations of local anaesthetic drugs for postoperative analgesia (as opposed to that required for surgery). If significant motor block develops, consider reducing the infusion rate and / or concentration of local anaesthetic.

If the block is too high (e.g. involving arms), reduce the rate of infusion and / or the concentration of local anaesthetic. If respiratory muscle weakness occurs, ventilation may be necessary until the effects of the local anaesthetic wear off.

At the doses used, the addition of opioids to epidural infusion may significantly improve analgesia without significant increase in the side-effect profile. Nausea and itching may be helped by low-dose naloxone without loss of analgesia. CNS depression may require ventilation.

Analgesia produced by regional blockade may mask the pain associated with the onset of lower limb complications such as compartment syndrome following trauma or limb surgery. Check distal limbs regularly for evidence of infection, pressure injuries and compartment syndrome.

Epidural techniques carry a small but serious risk of epidural haematoma or abscess formation, which if unrecognized, can lead to spinal cord compression and paralysis. In routine practice this risk is very small. In ICU patients, however, the risk may be higher because of the effects of coagulopathy and sepsis. The magnitude of this risk is unquantifiable, although overall it remains very low.

Box 14.2 Complications of epidural blockade

Local anaesthetics	Opioids
Potential local anaesthetic toxicity	Itching
Hypotension (sympathetic blockade)	CNS depression including apnoea
Muscle weakness (including respiration)	Urinary retention
Bradycardia (block > T4 level)	Nausea and vomiting
Urine retention
Complete or high spinal block (cardiovascular collapse, respiratory paralysis, loss of consciousness)

The use low concentration local anaesthetic agents in epidurals is intended to provide adequate analgesia whilst minimizing the risk of significant motor blockade. If profound motor block develops in a patient with a postoperative epidural, suspect possible spinal cord compression. Seek urgent advice.

Intrathecal drug adminstration

Be sure to understand the difference between epidural and intrathecal catheters. An epidural catheter is placed in the ‘epidural space’. This is a potential space deep to the ligamentum flavum but outside the layers of the dura. An intrathecal catheter is placed through the dura and arachnoid mater, and lies within the subarachnoid space, i.e. in the cerebrospinal fluid. An intrathecal catheter may be used for CSF drainage and pressure monitoring following neurosurgery, spinal surgery or thoracic aortic aneurysm repairs, and occasionally for intrathecal drug administration (rarely, continuous spinal anaesthesia).

Do not give drugs by the intrathecal route unless you have been specifically trained to do so. There have been a number of cases where incorrect drugs administered by this route have caused catastrophic and permanent neurological damage and death.

Common postoperative problems

Problems in the immediate postoperative period may include the effects of prolonged surgery, massive fluid / blood loss, sepsis, tissue ischaemia / reperfusion, delayed recovery from anaesthesia and the effects of the stress response to surgery and trauma.

Effects of prolonged surgery

Anaesthesia and surgery may be prolonged because of the extensive nature of the procedure or because of technical complexity. Problems may include hypothermia, atelectasis, dehydration and fluid loss, anaesthetic drug accumulation, and the effects of pressure, including the development of compartment syndromes. This phenomenon has re-emerged recently following prolonged robotic surgery. (See Hypothermia, p. 224, and Peripheral compartment syndromes, p. 319.)

Delayed recovery of consciousness

The causes of delayed recovery of consciousness following anaesthesia are often multifactorial. It may be impossible to determine initially which is the predominant problem. Factors that may contribute are shown in Box 14.3.

Box 14.3 Factors that may contribute to delayed recovery from anaesthesia

Residual effects of anaesthetic drugs

Metabolic encephalopathy

Most patients with delayed recovery of consciousness require a period of supportive care on ICU. A CT scan of the brain and EEG may be helpful to exclude significant intracranial pathology. In most cases the problem will resolve gradually over hours or days.

Prolonged neuromuscular block

Muscle relaxants are used extensively in anaesthesia to facilitate tracheal intubation, provide relaxation for surgical procedures, and allow lighter planes of general anaesthesia. In the ICU, patients are usually left to clear muscle relaxants without use of reversal agents. Following anaesthesia, the recovery of neuromuscular function is often hastened by the use of anticholinesterase drugs (e.g. neostigmine). These increase the concentration of acetylcholine at the neuromuscular junction and reverse the effects of non-depolarizing neuromuscular blocking drugs (competitive antagonists at the acetylcholine receptor). They are used in combination with glycopyrrolate, which reduces the undesirable (muscarinic) effects of acetylcholine. Typical doses are:

neostigmine 2.5 mg + glycopyrrolate 0.5 mg.

Problems relating to residual neuromuscular blockade have become less common since the introduction of newer shorter-acting drugs such as atracurium. Occasionally, however, there may be delayed recovery of neuromuscular function. Factors that may contribute to this are shown in Box 14.4.

Box 14.4

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