Tag Archives: sfgh

SFGH 5.31 pearls: metabolic alkalosis

  • 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!
  • 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
  • Betahydroxy butyrate can be elevated in any ketotic state, not just DKA
  • Severe alkalemia can also cause seizure, agitation/disorientation, and coma due to decreased cerebral blood flow
  • Fun fact – the combination of 3 concomitant acid-base disorders is known as “the triple ripple”!
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SFGH 5.25 am report pearls: thyrotoxic periodic paralysis

  • DDX Myopathy with low CK: steroid myopathy, hyperthyroidism, rheum disease (RA, lupus)

Hyperthyroidism associated neurologic manifestations:

  • Hyperthyroidism associated myopathy: expect proximal muscle weakness with normal serum CK
  • Oftentimes see a axonal sensory polyneuropathy, rarely a demyelinating polyneuropathy

 

Thyrotoxic periodic paralysis

  • Form of hypokalemic periodic paralysis, often associated with hyperthyroidism
  • Channelopathy characterized by episodes of painless muscle weakness
  • May be triggered by exercise, fasting, high carb meals (release of epinephrine or insulin)
  • More common in young Asian males (>95% of cases in men; 0.1 % in general population with hyperthyroidism, 2% in Asians with hyperthyroidism)
  • Weakness: Proximal>distal muscles, legs>arms
  • Associated with ictal (during the paralysis period) hypokalemia
  • Management: low dose potassium supplementation (high chance rebound hyperkalemia), IV propranolol
  • Prevention: restore euthyroidism, beta blockade

 

Great website for neurology learning:  http://neuromuscular.wustl.edu

Pothiwala P, Levine SN. Analytic review: thyrotoxic periodic paralysis: a review. J Intensive Care Med 2010; 25:71.

SFGH 5.23 pearls: Alc hep and KS

  • Patients with alcoholic hepatitis typically have a history of daily alcohol use and often will stop drinking as they start to feel ill (as in the case for this patient)
  • Common symptoms include jaundice, anorexia, RUQ pain, abdominal distension and fever, and those with severe alc hep may also have encephalopathy
  • Without treatment, patients with severe alc hep (DF ≥32) have a 30-day mortality of 25-45%, most commonly from GI bleeding, sepsis or liver failure
  • Treatment with steroids has been shown to improve mortality for those with severe alc hep, though steroids may be contraindicated if there is concern for GI bleeding, infection, or renal failure.
  • For severe alc hep with contraindications to steroids, pentoxifylline is an alternative, though data is weaker than for steroids and it has not been definitely shown to improve mortality (STOPAH trial from NEJM attached)
  • Supportive care with nutrition, PPI and abstinence from alcohol are also important!
  • If there is no improvement after 1 week of therapy based on the Lille score, ongoing treatment is not recommended and thought to have little benefit.
  • Kaposi’s sarcoma is an angioproliferative disorder due to HHV-8 infection. Most of the cases we see are AIDS-associated, but KS can also present with older men without HIV, in transplant patients, and among sub-Saharan African populations where there are endemic forms.
    • KS is the most common tumor among people with HIV
  • Cutaneous disease is most common, but it can be observed in any visceral organ, mostly commonly the mouth, GI tract and lungs.
    • Steroids are associated with induction and exacerbation of KS in HIV patients and other with underlying immunosuppression

5.9 ZSFG pearls: lung abscesses and gram positive rods

  • An uncomplicated parapneumonic effusion is characterized b normal glucose, normal pH and low cell count, and these normally will layer out with a lateral decub CXR (“simple” or free’ flowing” is the radiologic description)
    • These may subsequently become complicated effusions with thickening and formation of loculations and empyema. If this persists for weeks, the empyema may form a thick “pleural peel”
  • Empyemas are now rare complications of CAP (around 1% of cases) and bacteria associated with aspiration are the most common cause (strep milleri is the most commonly cultured pathogen)
  • Lung abscesses are another CAP complication commonly associated with aspiration
    • Most abscesses are managed conservatively with prolonged antibiotics, but more aggressive intervention should be pursued in patients who are elderly, have a large cavity, a long duration of symptoms prior to therapy, lower lobe abscesses or multiple abscesses (this patient had all of these!)
      • Remember to involve all the pertinent services in these cases, including pulm, IR and CT surgery

 

BPF pearls from last month:

  • Post-operative complications are by the far the most common cause of bronchopleural fistula, which is a very rare condition, but other etiologies include lung necrosis due to infection, persistent pneumothorax, radiation and TB.
  • Symptoms can mimic TB and include fever, productive cough and hemoptysis
  • The two main treatment strategies are mechanical plugs (with a balloon, gel foam, sclerosants, etc) and placement of a one-way valve.

 

 

Friday catch up pearl – Sanjay Saint’s mnemonic for remember the gram-positive rods:

Clumsy – Clostridium

Bacteria – Bacillus anthracis

Act – Actinomyces

Like – Listeria

Lazy – Lactobacillus

Error-prone – Erisipelothrix

Cornballs – Corynebacterium

 

https://www.evernote.com/shard/s300/sh/2cbdbd27-a42e-42ea-b612-e8c283563292/d6aff45a12d1702de1781f64359a27c9

 

5.4 SFGH am report pearls: coccidioidomycosis

 

  • clinical manifestations: often 7-21 days after exposure, although can reactivate later
    • asymptomatic in ~50%, CAP, arthralgias, e nodosum, e multiforme
  • diagnosis:
    • keep in mind epidemiology
    • cocci immunodiffusion (IgM vs IgG) is qualitative
    • Cocci complement fixation is quantitative and correlates with disease activity
      • Titer >1:16 = aggressive pulmonary disease OR disseminated disease
    • additional testing options include culture and PCR on fixed tissue
    • About 25% of patients with cocci will have >5% peripheral eosinophilia
  • Treatment is not always necessary, but should treat if >10% wt loss, persistent night sweats x 3wks, complement fixation titers >1:16, inability to work, HIV, or sx > 2 mos
    • Individuals of African or Philippine descent have an increased risk of extrapulmonary complications
  • Treatment is fluconazole or itraconazole x 3-6mos
  • Saubolle MA, McKellar PP, Sussland D. Epidemiologic, clinical, and diagnostic aspects of coccidioidomycosis. J Clin Microbiol 2007; 45:26.
  • Pappagianis D, Lindsay S, Beall S, Williams P. Ethnic background and the clinical course of coccidioidomycosis. Am Rev Respir Dis 1979; 120:959.
  • Galgiani JN, Ampel NM, Blair JE, et al. Coccidioidomycosis. Clin Infect Dis 2005; 41:1217.
  • Evernote link: http://www.evernote.com/l/AoNVmLN-TGBK4KBmmLlBeNVBI-1YzvA-1NE/

SFGH 5.2 pearls: Endometrial CA and pulm nodules

  • Endometrial carcinoma is the most common gyn malignancy in developed countries, with the main risk factor being excess estrogen (endogenous from obesity or exogenous hormone replacement therapy with estrogen)
    • Survival depends on stage, with stage IV survival at 5 year between 20-60%
  • Most cases present with uterine bleeding, and screening for asymptomatic women is not recommended except in women with Lynch syndrome
    • Pap smear is only about 50% sensitive for uterine cancer
    • Most women have disease confined to the uterus on diagnosis (68%)
    • Remember that CT is not a good imaging modality for uterine abnormalities – pelvic or transvaginal ultrasound is more sensitive, though endometrial cancer can only be diagnosed with tissue (EMB or hysterectomy sample)
  • Cocci testing – immunodiffusion for cocci IgM and IgG is a very specific, but not very sensitive test, as not all exposed patients will develop antibodies and antibody formation can lag behind the clinical presentation.
    • If either IgM or IgG immunodiffusion tests are qualitatively positive, complement fixation should be done subsequently for quantitative analysis
    • Comp fix is often called “the IgG test”! This test provides titers based on depletion of compliment that results when cocci antibodies and antigen form an immune complex in an infected patient
      • Most patients with extrapulmonary cocci have comp fix titers of 1:16 or greater
  • Histo is most common in Central and North America, with the North American hot spots including the Ohio and Mississippi River valleys.
    • Pulmonary histo should be on your ddx for patients with mediastinal or hilar LAD or masses, pulmonary nodules, cavitary lung lesions, and pulm symptoms with arthritis/arthralgia and erythema nodosum and often shares a ddx with TB, sarcoid and lung cancer
      • It’s important to rule out histo when you’re considering a sarcoid diagnosis, as giving steroids for sarcoid in a patient who actually has histoplasmosis can lead to disseminated infection

4. 29 am report pearls: Alcohol related Cirrhosis

 

  • cirrhosis related to viral hepatitis is characteristically a small, shrunken liver
  • cirrhosis related to EtOH use is usually characterized by hepatomegaly
  • How much alcohol?
    • a man drinking 80 grams of alcohol daily will, on average, develop cirrhosis of the liver in 10 years
    • a woman drinking 80 grams daily of alcohol will, on average, develop cirrhosis in 5 years
      • one pint of wine, 3 12 oz beers, or 4 oz of distilled spirits is 20-40 grams of alcohol
      • the term “fifth of vodka” refers to when bottles were 4/5 of a quart which = 1/5 of a gallon.  Now we no longer measure bottles by the gallon, but 1/5 of a gallon is very close to 750 ml bottles
  • ferritin production is increased in the inflammatory state of alcoholic liver disease and acute or subacute hepatitis (from any cause).  In addition alcohol suppresses liver transferrin synthesis, elevating the serum transferrin saturation in alcoholic liver disease.
    • on biopsy, hepatic iron levels in those with alcoholic liver disease are relatively normal, especially in comparison to those with hemochromatosis

O’Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307.

Bird GL, Williams R. Factors determining cirrhosis in alcoholic liver disease. Mol Aspects Med 1988; 10:97.

Chapman RW, Morgan MY, Laulicht M, et al. Hepatic iron stores and markers of iron overload in alcoholics and patients with idiopathic hemochromatosis. Dig Dis Sci 1982; 27:909.

 

Evernote link: http://www.evernote.com/l/AoO_nJBWLMdAyqgelL3_IOXlVjuuZhhsug0/