emergencies Flashcards
what do we give for suspected meningococcal disease
dose of benzylpenicillin should be given either intramuscularly (or intravenously if IV access is present)
features of henoch-scholein purpura
purpura is typically symmetrical, over extensor surfaces and over the legs and buttocks
joint pain and swelling abdominal pain
Acute meningococcaemia description
A serious communicable infection transmitted via respiratory
secretions; bacteria get into the circulating blood
cause of acute meningoccaemia
● Gram negative diplococcus Neisseria meningitides
presentation of acute meningoccaemia
● Features of meningitis (e.g. headache, fever, neck stiffness),
septicaemia (e.g. hypotension, fever, myalgia) and a typical rash
● Non-blanching purpuric rash on the trunk and extremities, which
may be preceded by a blanching maculopapular rash, and can
rapidly progress to ecchymoses, haemorrhagic bullae and tissue
necrosis
Complications of acute meningococcaemia
- Septicaemic shock
- disseminated intravascular coagulation
- multi-
organ failure - death
what is TEN
Toxic epidermal necrolysis (TEN) is a potentially life-threatening skin disorder that is most commonly seen secondary to a drug reaction
features of TEN
systemically unwell e.g. pyrexia, tachycardic
positive Nikolsky’s sign: the epidermis separates with mild lateral pressure
drugs that induce TEN
phenytoin sulphonamides allopurinol penicillins carbamazepine NSAIDs
management for TEN
- stop precipitating factor
- supportive care, often in intensive care unit
- other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis
causes of urticaria, angioedema and anaphylaxis
Idiopathic, food (e.g. nuts, sesame seeds, shellfish, dairy
products), drugs (e.g. penicillin, contrast media, non-steroidal antiinflammatory drugs (NSAIDs), morphine, angiotensin-converting
enzyme inhibitors (ACE-i)), insect bites, contact (e.g. latex), viral or
parasitic infections, autoimmune, and hereditary (in some cases of
angioedema)
pathophysiology of urticaria
a local increase in permeability of capillaries
and small venules. A large number of inflammatory mediators
(including prostaglandins, leukotrienes, and chemotactic factors)
play a role but histamine derived from skin mast cells appears to
be the major mediator. Local mediator release from mast cells can
be induced by immunological or non-immunological mechanisms.
presentation of urticaria
swelling involving the superficial dermis, raising the
epidermis): itchy wheals
presentation of angiooedema
(deeper swelling involving the dermis and
subcutaneous tissues): swelling of tongue and lips
presentation of anaphylaxis
bronchospasm,
facial and laryngeal oedema, hypotension; can present initially
with urticaria and angioedema
