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
Mx of urticaria, anaphylaxis, angioedema
● Antihistamines for urticaria
● Corticosteroids for severe acute urticaria and angioedema
● Adrenaline, corticosteroids and antihistamines for anaphylaxis
complications of urticaria, angioedema, anaphylaxis
● Urticaria is normally uncomplicated
● Angioedema and anaphylaxis can lead to asphyxia, cardiac arrest
and death
what is erythema nodosum
● A hypersensitivity response to a variety of stimuli
inflammation of subcutaenous fat
causes of erythema nodosum
● Group A beta-haemolytic streptococcus, primary tuberculosis,
pregnancy, malignancy, sarcoidosis, inflammatory bowel disease
(IBD), chlamydia and leprosy
Drugs - pencillin, sulphonamides, COCP
presentation of erythema nodosum
● Discrete tender nodules which may become confluent
● Lesions continue to appear for 1-2 weeks and leave bruise-like
discolouration as they resolve
● Lesions do not ulcerate and resolve without atrophy or scarring
● The shins are the most common site
description of erythema multiforme
acute self-
limiting inflammatory condition with herpes simplex virus being
the main precipitating factor. Other infections and drugs are also
causes. Mucosal involvement is absent or limited to only one
mucosal surface.
description of erythema multiforme
acute self-
limiting inflammatory condition with herpes simplex virus being
the main precipitating factor. Other infections and drugs are also
causes. Mucosal involvement is absent or limited to only one
mucosal surface.
Complications
sepsis
electrolyte imbalance
multisystem organ failure
Complications of erythema multiforme, SJS, TEN
sepsis
electrolyte imbalance
multisystem organ failure
what is necrotising fascitis
A rapidly spreading infection of the deep fascia with secondary
tissue necrosis
causes of necrotising fascitis
● Group A haemolytic streptococcus, or a mixture of anaerobic and
aerobic bacteria
● Risk factors include abdominal surgery and medical co-morbidities
(e.g. diabetes, malignancy)
presentation of necrotising fascitis
● Severe pain
● Erythematous, blistering, and necrotic skin
● Systemically unwell with fever and tachycardia
● Presence of crepitus (subcutaneous emphysema)
● X-ray may show soft tissue gas (absence should not exclude the
diagnosis)
presentation of necrotising fascitis
● Severe pain
● Erythematous, blistering, and necrotic skin
● Systemically unwell with fever and tachycardia
● Presence of crepitus (subcutaneous emphysema)
● X-ray may show soft tissue gas (absence should not exclude the
diagnosis)
Mx for necrotising fascitis
● Urgent referral for extensive surgical debridement
● Intravenous antibiotics
complications of erythema nodosum
encapsulated fat necrosis
