6.19 AM report pearls at SFGH – Metabolic Alkalosis

 
Take away points from the case:

·         Major causes metabolic alkalosis – Vomiting/NG suction, loop and thiazide diuretics, laxative abuse, mineralocorticoid excess, milk-alkali syndrome.
·         For those with profound alkalosis with hypovolemia, avoid resuscitation with plasmalyte, as it contains bicarb. Better to replete with NS w/K or just NS and replete K separately
·         Profound alkalemia also can cause a left shift of the oxygen dissociation curve, leading to impaired peripheral oxygen unloading and lactate elevation à give supplemental oxygen!
Other pearls from the morning for your reading/teaching pleasure:
·         An elevated serum pH requires both an initial insult, (usually loss of hydrogen ions in the urine or GI tract) and a maintenance phase that prevents normalization of the pH. The maintenance phase causes include: volume contraction, renal impairment, decreased effective blood volume (CHF, cirrhosis) or a combination of these factors.
·         Remember that alkalemia drives phosphorus and potassium into cells, so labs will often show profound hypoK and hypo phos, but these numbers do not reflect total body stores.
·         The lytes abnormalities associated with alkalemia can lead to muscle weakness, decreased cardiac contractility and increased risk for arrhythmia and should be corrected as soon as possible, keeping in mind that their extra-cellular levels will change as your correct the pH
·         Severe alkalemia can also cause seizure, agitation/disorientation, and coma due to decreased cerebral blood flow
·         Profound alkalemia also can cause a left shift of the oxygen dissociation curve, leading to impaired peripheral oxygen unloading and lactate elevation à give supplemental oxygen!
·         Fun fact – the combination of 3 concomitant acid-base disorders is known as “the triple ripple”!
 
From the images (one showing an extremely dilated esophagus from achalasia and one showing severe bamboo spine from longstanding ankylosing spondylitis)
·         When starting TNF inhibitors, screen for TB and hep B, as both can flare after treatment initiation. About 50% of TB cases that flare with TNF inhibitors are extrapulmonary
·         The most common CXR findings in achalasia is a widened mediastinum due to esophageal dilation. Some may also lack a gastric air bubble because the contracted LES prevents air passage into the stomach.
·         SI joint abnormalities in ankyloses spondylitis may be apparent on MRI before they are appreciable on plain films
·         Early findings of AS may show widening of the SI joints because of the active inflammation, but later stages with show narrowing of the spaces and ultimately fusion.
·         The bamboo spine in the end stage of AS and represents complete fusion of the vertebral bodies
 
Evernote Link!
 
 
http://www.anaesthesiamcq.com/ – An awesome anesthesia book with great acid-base physiology info, among other useful topics 
 
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