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40. POST ANAESTHETIC CARE UNIT COMPLICATIONS
The incidence of post anaesthetic/surgery
complications varies but has been estimated to occur in approximately 5% of
patients. The most common complications are nausea and vomiting, hypotension,
hypertension, arrhythmias, altered conscious state and respiratory depression.
All patients should be observed in a post anaesthetic care unit till they are
well enough to return to the ward.
CARDIOVASCULAR COMPLICATIONS
Hypotension
The accuracy of the blood pressure should be
checked. In all cases the patient’s airway must be assessed and oxygen administered.
Check the patient’s pulse. Bradycardia and tachycardia can cause hypotension.
Obtain an ECG. Bradycardia may need up to 3 mg of atropine in 0.5 mg doses.
Raising the patient’s legs will improve
venous return.
Hypovolaemia is the most common cause of hypotension in the PACU.
Intravenous fluid (250 to 1000 ml) should be given whilst the anaesthetist
reviews the patient’s history, anaesthetic and surgical history and examines
the patient. Remember to check drains and dressings for blood loss. If the
hypotension is not corrected by adequate volume replacement the anaesthetist
must look for other causes of hypotension.
Other causes of hypotension include decreased
vascular tone, decreased venous return due to mechanical forces and decreased
myocardial activity.
There are several causes of decreased
vascular tone including anaesthetic
agents, spinal/epidural anaesthesia, anaphylaxis and infection. These patients
need fluid replacement and drug treatment with alpha-receptor agonists such as
metaraminol, epinephine (adrenaline) or norepinephine (noradrenaline).
Decreasing the force of contraction of the
heart (decreased inotropy) will
cause hypotension. There are many causes of decreased inotropy including
myocardial ischaemia, myocardial infarction, arrhythmias, cardiac failure,
drugs, infection and hypothyroidism. The anaesthetist must examine the patient
for signs and symptoms and treat any cause. A 12 lead ECG and basic laboratory
investigations may help in the diagnosis.
Mechanical causes of decreased venous return
are unusual and include pneumothorax
and pericardial tamponade. These
patients will have signs of hypovolaemia (hypotension, tachycardia, dry mucous
membranes, thirst, decreased urine output, decreased conscious state) and signs
of obstruction to venous return (jugular vein distention, elevated central
venous pressure, decreased breath and heart sounds). They also need volume
replacement. The cause of the mechanical obstruction must be treated.
Hypertension
When hypertension occurs it is often caused
by pain, hypercapnia, hypoxia,
full urinary bladder or excessive
intravenous fluid administration.
Hypertension may also occur in patients with pre-existing hypertension especially if they have not received their usual
anti-hypertensive medications.
The anaesthetist must check the accuracy of
the blood pressure reading, administer oxygen, assess the patient’s airway,
review the patient’s medical and surgical history and examine the patient.
Management aims at treating the cause and the
hypertension. There are many drugs that are suitable for treating hypertension
in the PACU including beta-adrenergic blockers, calcium channel blockers,
hydralazine and nitrates.
Dysrhythmias
The causes of dysrhythmias include hypoxia, hypercarbia, pain, electrolyte
imbalance (especially hypokalaemia), drugs acid-base imbalance and myocardial ischaemia.
The anaesthetist must assess the patient’s
airway, give oxygen and check the patient’s blood pressure. Patients who are
hypotensive, hypoxic or have signs of myocardial ischaemia need immediate
treatment.
The most common dysrhythmias in PACU are
sinus tachycardia, sinus bradycardia, premature ventricular beats, ventricular
tachycardia and supraventricular tachycardia.
Sinus tachycardia may be caused by pain, hypoxia, hypercarbia,
hypovolaemia, infection, cardiac failure or pulmonary embolism. The
anaesthetist must treat the cause of the sinus tachycardia.
Sinus tachycardia can occur from a high
spinal block, drugs and vagal stimulation. The anaesthetist should administer
oxygen and check the blood pressure. Patients with bradycardia and hypotension
need immediate treatment with atropine or adrenaline and intravenous fluid
replacement depending on the severity.
Supraventricular tachycardia (SVT) has many causes including hypoxia, hypercarbia, acid
base disturbances, electrolyte abnormalities, hyperthyroidism and valvular
heart disease. The supraventricular tachycardia may arise from the sino-atrial
node, atrium or atrio-ventricular node. The anaesthetist must assess the
patient’s airway, administer oxygen and check the blood pressure. If the
patient is not hypotensive the anaesthetist should try to diagnose the SVT.
Diagnosis is made easier by slowing the ventricular rate (carotid body massage,
adenosine 3 to 6 mg intravenously). If hypotension is severe the anaesthetist
should give a vasopressor and consider immediate cardioversion. Atrial
flutter can be treated with esmolol
10 mg intravenously, digoxin 0.25 mg intravenously or cardioversion 10 to 25 J
if necessary. Atrial fibrillation
can be treated with digoxin 0.5mg intravenously, verapamil 2.5 to 5 mg
intravenously, esmolol 10mg intravenously or cardioversion 100 to 200 J.
Re-entry tachycardia (including Wolff-Parkinson-White syndrome) can be treated with adenosine 3 to 6 mg
intravenously or verapamil 2.5 to 5 mg intravenously up to a total of 20 mg.
Avoid using calcium channel blocking drugs and beta blocking drugs together as
they can cause severe hypotension.
Ventricular tachycardia has many causes including hypoxia, myocardial
ischaemia, acidosis and hypokalaemia. The anaesthetist must assess the
patient’s airway, administer oxygen and check the blood pressure. If the
patient is hypotensive they need immediate cardioversion. Stable ventricular
tachycardia can be treated with lignocaine 1.5 mg/kg intravenously, followed by
an infusion at 1 to 4 mg/min.
Myocardial Ischaemia
The anaesthetist must correct any imbalance
between myocardial oxygen demand and myocardial oxygen supply. Common causes
include hypoxaemia, anaemia, tachycardia, hypotension and hypertension and must
be treated.
RESPIRATORY COMPLICATIONS
The anaesthetist must assess the patient’s
airway and establish a clear upper airway. The patient may need a “jaw thust”,
oropharyngeal/nasopharyngeal airway, assisted mask ventilation or endotracheal
intubation. Oxygen must be given. The anaesthetist should also check and treat
the patient’s blood pressure and heart rate.
Hypoxaemia
General anaesthesia has several physiological
effects that continue in the postoperative period that can cause
hypoventilation and hypoxaemia. General anaesthesia causes a reduction in the
functional residual capacity, inhibits hypoxic pulmonary vasoconstriction,
inhibits hypoxic and hypercarbic ventilatory drive and decreases respiratory
muscle strength.
Causes of hypoxaemia include pneumothorax, aspiration of gastric contents, bronchospasm, laryngospasm, upper airway obstruction, hypoventilation, pulmonary oedema and diffusion hypoxia.
Hypoxia must be excluded before giving a
sedative to calm a patient. Sedatives (e.g. benzodiazepines) are rarely needed
in recovery.
Hypoventilation
Decreased ventilatory drive or weak
respiratory muscles can cause hypoventilation. Hypoventilation will cause
hypoxia, hypercarbia and eventually, apnoea and myocardial ischaemia. The
anaesthetist must assess the patient’s airway breathing and circulation. The
anaesthetic history, medical history and examination of the patient may
diagnose the cause.
Decreased ventilatory drive can be caused by anaesthetic agents (inhalation agents, narcotics, benzodiazepines).
Naloxone will reverse hypoventilation due to opioids. Doses of 100 micrograms
will treat the hypoventilation in 1 to 2 minutes and last 30 to 60 minutes. Naloxone has several side-effects including tachycardia,
hypertension, pulmonary oedema and pain. Doses of flumazenil, 0.2 mg will reverse the hypoventilation caused by
benzodiazepines.
Weak respiratory muscles may be from pre-existing respiratory disease or inadequate reversal of neuromuscular blockade. In most cases neuromuscular blockers should be
reversed (neostigmine 2.5 mg plus atropine 1.2 mg). Neuromuscular blockade
should be monitored during the operation with a peripheral nerve stimulator if
available.
Clinical signs of inadequate reversal include
hypoxia, shallow breathing, generalised twitching and patient distress. If
adequately recovered from neuromuscular blocking drugs, the patient should be
able to lift their head off the pillow for 5 seconds.
Upper Airway Obstruction
The anaesthetist must immediately treat upper
airway obstruction and give oxygen. Patients will show signs of inadequate
respiration, intercostal and suprasternal retraction and abnormal chest and
abdominal movement. Patients may require a nasopharyngeal/oropharyngeal airway,
assisted manual ventilation or endotracheal intubation.
Upper airway obstruction can be caused by incomplete
recovery from anaesthesia, laryngospasm,
foreign body or airway oedema.
The most common cause of upper airway obstruction
is pharyngeal obstruction from a sagging tongue in the unconscious patient.
This is most effectively treated by tilting the patient’s head backwards and
moving the jaw forwards or moving the patient to a lateral position.
CENTRAL NERVOUS SYSTEM COMPLICATIONS
Failure to Regain Consciousness
The anaesthetist must check that the patient
has a clear airway, is breathing and has an adequate blood pressure and heart
rate. Oxygen should be given.
The most frequent cause of delayed awaking is
the persistent effect of anaesthesia.
The anaesthetist must assess the patient and anaesthetic history. Drugs such as
naloxone and flumazenil will reverse some of the sedative effects of
anaesthesia.
Other causes include decreased cerebral
perfusion, hypoxaemia, metabolic causes such as hypoglycaemia, sepsis,
severe hypothermia, hyponatraemia and other electrolyte, and acid base disturbances. Cerebrovascular accidents and raised intracranial pressure are rare causes of delayed awakening.
Emergence Delirium
Delirium is more common in the elderly and
patients with a history of alcohol abuse and dementia but there are several
other causes including hypoxaemia, acidosis, hypoglycaemia, sepsis, raised
intracranial pressure, hyponatraemia and severe pain.
Postoperative Nausea and Vomiting
Postoperative nausea and vomiting (PONV) is common after surgery. Untreated, at least one
third of patients who undergo surgery will have postoperative nausea and
vomiting. Numerous pathophysical mechanisms are known to cause nausea and
vomiting. Nausea and vomiting may be caused by visceral stimulation though
dopamine and serotonin, by vestibular and central nervous system stimulation
though histamine and acetylcholine, and by chemoreceptor trigger zone
stimulation though dopamine and serotonin.
Volatile anaesthetics, nitrous oxide and
opioids increase the incidence of PONV. Using multi-modal analgesia can reduce
opioid doses. Intra-operative intravenous fluids can reduce postoperative
nausea and vomiting.
4 mg of ondansetron (or a similar serotonin
antagonist), 4 mg of dexamethasone, 1.25 mg of droperidol and total intravenous
anaesthesia all reduce the relative risk of PONV to a similar extent
(approximately 26 percent). These interventions all act independently of one
another. Metoclopramide is probably ineffective prophylactically. Dexamethasone
should be given at the start of anaesthesia. Because the relative risk
reduction is similar the anaesthetist should choose the least expensive and
safest option first.
Prevention of PONV will provide the greatest
absolute risk reduction in patients with the greatest risk of PONV. The most
important risk factors are female, non-smoker and a history of motion sickness
and PONV and the use of postoperative opioids. Patients at high risk (3 or 4
risk factors) may benefit from a combination of interventions. Patients at
moderate risk (2 risk factors) may benefit from a single intervention.
Prophylaxis is rarely indicated for patients at low risk.
An antiemetic that has not been used
prophylactically should be chosen for the treatment of PONV.
Postoperative Hypothermia and Shivering
Hypothermia causes shivering and increases
metabolic rate, cardiac output and oxygen requirements (up to 500%). Patients
who shiver should receive oxygen and be warmed. 25 to 50 mg of intravenous
pethidine is usually effective for non-hypothermic shivering.
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