Kawasaki- Fever of ≥5 days' duration plus 4 of:
- Bilateral nonsuppurative conjunctivitis
- One or more changes of the mucous membranes of the upper respiratory tract
- Pharyngeal injection, dry fissured lips, injected lips, "strawberry" tongue
- One or more changes of the extremities
- Peripheral erythema, peripheral edema, periungual desquamation, generalized desquamation
- Polymorphous rash
- Cervical lymphadenopathy
- Need echocardiogram to exclude coronary artery aneurysm
Maculopapular
- Macules are small, flat discolored spots
- Papules are small, raised bumps
Mefenamic acid overdose
- Convulsions, nausea, emesis, haematemesis, bradypnea, coma
- Renal failure
- Onset of symptoms is usually between 30 minutes and 4 hours, but signs
of renal failure may appear several days after an overdose
- Lethal dose can be
as low as 2.5 g
- Conservative management; Can manage acidosis with bicarb
Sylvian fissure - AKA lateral sulcus
- Divides the frontal lobe and parietal lobe above from the temporal lobe below
- Longer in the left hemisphere in most people
- Dot sign = MCA embolus
Methemoglobinemia - PathPhys
- Higher than normal level of methemoglobin (metHb, i.e., ferric [Fe3+] rather than ferrous [Fe2+] haemoglobin) in the blood
- Methemoglobin has a decreased ability to bind oxygen, but allosterically raises affinity for the other 3 ferrous haemoglobins
- => Shifts dissociation curve to left => Tissue hypoxia
- Elevated levels of methemoglobin in the blood are caused when the mechanisms that defend against oxidative stress within the red blood cell are overwhelmed
- => Oxidation of ferrous iron
- Can give
the blood a bluish or chocolate-brown color
- Causes
- Congenital methemoglobinemia
- Autosomal recessive - due to a deficiency of the enzyme diaphorase I (NADH methemoglobin reductase)
- May also be seen in patients with abnormal hemoglobin variants such as hemoglobin M (HbM), or hemoglobin H (HbH)
- Not amenable to reduction despite intact enzyme systems
- Can also arise in patients with pyruvate kinase deficiency due to impaired production of NADH
- Patients with Glucose-6-phosphate dehydrogenase (G6PD) deficiency may have impaired production of NADPH
- Acquired
- Exposure to exogenous oxidizing drugs and their metabolites (benzocaine, dapsone, nitrates)
- e.g. Nitrates from farms in drinking water
- Other classical drug causes:
- Antibiotics (trimethoprim, sulfonamides, dapsone)
- Local anesthetics (especially articaine and prilocaine)
- Aniline dyes, metoclopramide, chlorates, bromates
- Management
- Supplemental oxygen and methylene blue
1% solution (10 mg/ml) 1 to 2 mg/kg slow IV
- Restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state
Notes
- Erythromycin for gastric stasis
- AmBisome = Amphotericin B
- Formoterol = LABA
- Clonidine
- Centrally acting α2 adrenergic agonist
- For HTN. ADHA, anxiety/panic disorder, pain
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