A Textbook of Clinical Pharmacology and Therapeutics

Table 53.2: Central nervous system effects of opioids
Analgesia
Euphoria
Drowsiness : sleep : coma
Decrease in sensitivity of respiratory centre to CO2 Depression of cough centre
Stimulation of chemoreceptor trigger zone (vomiting in
15% of cases)
Release of antidiuretic hormone
Table 53.3: Medical complications of opioid addiction
Infection Endocarditis – bacterial, often tricuspid valve,
staphyloccocal, fungal (e.g. Candida)
HIV/hepatitis B virus (HBV)/hepatitis C virus
(HCV)
Abscesses
Tetanus
Septicaemia
Hepatitis
Pulmonary Pneumonia – bacterial, fungal, aspiration
Pulmonary oedema – ‘heroin lung’
Embolism
Atelectasis
Fibrosis/granulomas
Skin Injection scars
Abscesses
Cellulitis
Lymphangitis
Phlebitis
Gangrene
Neurological Cerebral oedema
Transverse myelitis
Horner’s syndrome
Polyneuritis
Crush injury
Myopathy
Hepatic Cirrhosis
Renal Nephrotic syndrome with proliferative
glomerulonephritis
Musculoskeletal Osteomyelitis (usually lumbar vertebrae,
Pseudomonas, Staphylococcus, Candida),
crush injury, myoglobinuria, rhabdomyolysis
as a way of minimizing medical complications of opioid
dependence.
INTOXICATION AND OVERDOSE
For several seconds following intravenous injection, heroin
produces an intense euphoria (rush) which may be accompanied
by nausea and vomiting, but is nevertheless pleasurable.
Over the next few hours the user may describe a warm
sensation in the abdomen and chest. However, chronic users
often state that the only effect they obtain is remission from
abstinence symptoms. On examination, the patient may appear
to be alternately dozing and waking. The patient may be hypotensive
with a slow respiratory rate, pin-point pupils and infrequent
and slurred speech. These signs can be reversed with
naloxone. Opioids predispose to hypothermia.
Overdose is commonly accidental due to unexpectedly
potent heroin or waning tolerance (e.g. after release from
prison). Severe overdose may cause immediate apnoea, circulatory
collapse, convulsions and cardiopulmonary arrest.
Alternatively, death may occur over a longer period of time,
usually due to hypoxia from direct respiratory centre depression
with mechanical asphyxia (tongue and/or vomit blocking
the airway).
A common complication of opioid poisoning is noncardiogenic
pulmonary oedema. This is usually rapid in onset,
but may be delayed. Therefore, any patient who is admitted
following heroin overdose should usually be hospitalized for
approximately 24 hours. Naloxone reverses opioid poisoning
with a rapid increase in pupil diameter, respiratory rate and
depth of respiration. It may precipitate an acute abstinence
syndrome in addicts and (very rarely) convulsions. This does
not contraindicate its use in opioid overdoses in addicts.
Severe hypoxia causes mydriasis and some opioids (notably
pethidine) have an anti-muscarinic atropine-like mydriatic
effect, so absence of small pupils should not preclude a trial of
naloxone when the clinical situation suggests the possibility
of opioid overdose. Naloxone is eliminated more rapidly than
morphine and may need to be administered repeatedly
(Chapter 25).
TOLERANCE AND WITHDRAWAL
OPIOID/NARCOTIC ANALGESICS 435
Increasing doses of opioid must be administered in order to
obtain the effect of the original dose. Such tolerance affects the
euphoric and analgesic effects, so the addict requires more
and more opioid for his or her ‘buzz’. Changes in tolerance are
much less apparent in the therapeutic use of opioids for the
treatment of pain.
Withdrawal symptoms usually start at the time when the
next dose would normally be given, and their intensity is
related to the usual dose. For heroin, symptoms usually reach
a maximum at 36–72 hours and gradually subside over the
next five to ten days. Table 53.4 lists features of the opioid
abstinence syndrome.