14.02.03 ICU notes
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
Pimarily truncal
Cervical lymphadenopathy
>1.5 cm in diameter
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
IV antifungal
Formoterol = LABA
Clonidine
Centrally acting α2 adrenergic agonist
For HTN. ADHA, anxiety/panic disorder, pain