Tuesday, February 26, 2013


Today we had an interesting discussion on Asthma and it's potential mimicers, here is a synopsis:
  • Diagnosis:
    • FEV1/FVC less than0.75-0.8 with 12%+ improvement with beta-agonist
    • More than 20% variation in peak expiratory flow (PEF)
    • Methacholine challenge: PC20 (Concentration required for a drop in FEV1 of 20%) less than 4mg/ml
  • Measures of poor control:
    • Daytime symptoms more than 4/wk and night time symptoms more than 1/wk
    • Missing days of work/school
    • Decreased physical activity
    • Frequent exacerbations
    • FEV1 or PEF less than 90% of personal best
    • Need for fast-acting beta2 agonist more than 4 doses/wk
    • Sputum eosinophils more than 2-3%
  • Treatment of Asthma exacerbation:
    • Markers of severe disease/impending respiratory collapse:
      • Work of breathing: use of accessory muscles
      • Hypoxia (asthma is really a problem with ventilation, when oxygenation starts to decrease that's a worrisome sign)
      • Pulsus paradoxus greater than10mmHg
      • Silent chest!
    • Inhaled beta agonists: short acting beta 2-agonists (salbutamol, albuterol) and short acting anti-cholinergics (iptratropium) MDI with aerochamber
    • Prednisone: 40-60mg Prednisone daily or if unable to take PO consider IV solumedrol for 10-14 days.
    • Adjuncts: MgSO4 2mg IV, Leukotriene receptor antagonists
    • Intubation if needed
    • Abx if evidence of pneumonia 
  • Complications of asthma that may present as worsening/non-responding asthma:
    • Churg-Strauss: Medium-small vessel vasculitis that presents with worsening asthma, eosinophilia and ANCA positive in 40-60%. Other signs of vasculitis include: leukocytoclastic vasculitis (palpable purpura), mononeuritis mulitplex and less commonly RPGN.
    • ABPA: Allergic bronchopulmonary aspergillosis. Major diagnostic criteria:
      • Hx of asthma
      • New pulmonary infiltrate
      • Immediate skin sensitivity to aspergillus precipitins
      • Precipitating serum antibodies to A. fumigatus
      • Peripheral eosinophilia (500/mm3)
      • IgE (1000ng/ml)
      • Increased serum antibodies IgG, IgA, IgE
      • Central bronchiectasis
    • Cryptogenic Organizing pneumonia (previously called BOOP):
      • A non-specific pulmonary inflammatory process manifesting as inflammation of the distal bronchioles, alveolar ducts/walls. Characterized by fever, malaise, chronic cough, areas of infiltration in CXR
      • Terminology: Organizing pneumonia of determined cause and if it is "idiopathic" it is referred to as organizing pneumonia of undetermined cause or COP
      • Causes of organizing pneumonia: infections (including: mycoplasma, PJP, HIV, cryptococcus), drugs (amiodarone, cocaine, bleomycine), malignancy.
      • Can also occur in the context of CTD: SLE, sjogren's, dermatomyositis, etc.
  • Mimicers of Asthma:
    • Paradoxical vocal cord motion: the vocal cords move in during inspiration. Can be triggered by stress, exercise, airway manipulation, irritant inhalations. Presents with upper airway stridor, throat tightness, hoarseness cough. Treat with reassurance and asking the patient to "pant"
    • Laryngospasm: Can be induced by URTI, presents with aphonia and choking sensation. Use of continuous positive airway pressure and heliox may help.
    • "Cardiogenc wheeze": Don't miss the patient who presents with wheeze secondary to pulmonary edema (cardiogenic or non-cardiogenic)!

Thursday, February 21, 2013

C. Difficile Colitis

1) Risk factors:
  • Age >65yrs
  • Recent antibiotic use (all and any abx use will put patients at risk for C. diff but increased risk if multiple abx and prolonged use)
  • Recent hospitalization or residence in a nursing home/health care facility
  • Treatment with PPI
  • Comorbidities (DM, liver disease, CKD, cancer on treatment, solid organ transplant)
2) C. Diff treatment from the IDSA guidelines:
  • Initial episode, mild/moderate
    • WBC less than 15, Creat less than 1.5 x baseline
    • Treat with metronidazole 500mg PO TID x 10-14 days
  • Initial episode, severe 
    • WBC greater than 15, Creat greater than 1.5 x baseline
    • Treat with Vancomycin 125mg PO QID x 10-14 days
  • Initial episode, severe + complicated
    • WBC greater than 15, Creatinine greater than 1.5 x baseline
    • PLUS toxic megacolon, ileus, shock
    • Vanco 500mg PO QID and consider rectal instillation if ileus
    • IV Metronidazole 500mg Q8H
    • Surgical consult
  • Initial recurrence
    • Classify as mild/moderate/severe/complicated and treat appropriately
    • Ok to treat with metronidazole if mild disease, however avoid prolonged metronidazole to avoid neurotoxicity
  • Second recurrence
    • Treat according to severity, otherwise treat with Vancomycin 125mg PO QID with a tapered regimen
  • See the IDSA guidelines for more details: IDSA Clinical Treatment guidelines for C. diff 2010
2) Diagnosis of Toxic Megacolon:
  • Etiology: IBD, infectious (c. diff, CMV, shigella, salmonella, e.coli, etamoeba histiolytica etc.)
  • Diagnosis: 
    • Radiographic findings (greater than 10cm) 
    • At least three of: fever, elevated WBC, tachycardia, anemia, dehydration, altered sensorium, electrolyte abN, hypotension.
  • Treatment: 
    • Surgical consult!
    • Medical Mx: ICU admission, NG tube for decompression, restart eteral feeding as soon as symptoms improve, consider IV steroids in IBD associated toxic megacolon
See this link for further information: Clostridium dificille infection Mayo Clinic Proceedings 2012

Wednesday, February 20, 2013



Causes of hypercalcemia:
1) PTH mediated: 
  • Primary- sporadic
  • Secondary - Chronic renal failure
  • Teritary - post renal transplant - autonomous production from hypertrophied parathyroid glands
2) Non-PTH mediated
  • Malignancy mediated:
  1. PTH rP - SCC (lung, H+N), solid tumours (renal, breast, bladder, ovarian)
  2. Lymphoma - from activation of extra-renal 1-alpha OH and production of calcitriol
  3. Bony mets: Osteoblastic (prostate, carcinoid, SCLC, hodgkins), osteolytic (myeloma, RCC, nonSCLC, NHL, melanoma)
  • Non-malignancy related
  1. Granulomas: Sarcoid, TB (activation of extra-renal 1-alpha OH and production of calcitriol)
  2. Paget's disease: Regional areas of accelerated rate of bone remodelling resulting in abnormal bone architecture, bony pain, fractures and hypercalcemia.
  3. Immobilization (often concomitant with another cause of hypercalcemia)
  4. Medications: Thiazide, lithium
  5. Endocrine: Hyperthyroidism, adrenal insufficiency
  6. Milk alkali
  • Moans: Abdominal pain/constipation, nausea, anorexia
  • Bones: Bony pain
  • Groans: Calcium kidney stones (CaPhos or Caoxalate)
  • Psychic overtones: Change in LOC, delirium
  • The cornerstone of treatment is: FLUIDS, FLUIDS, FLUIDS. Patients are often quite hypovolemic secondary to their inability to concentrate urine and nephrogenic diabetes insipidus. The kidneys should be able to excrete the majority of excess calcium  
  • Calcitonin:  4u/kg IM/SC rapid reduction in serum Ca by 1-2mmol/L. Works in 4-6 hrs.  
  • Bisphosphonates:  Pamidronate 30mg, 60mg, 90mg IV. More sustained reduction in Ca, takes 1-2 days to start working.  
  • Lasix:  Caution as this can cause worsening hypercalcemia from hypovolemia. Only used of pt is showing signs of volume overload from fluid resuscitation. see article from Annals of Internal Medicine: Furosemide from Hypercalcemia: An unproven yet common practice

Friday, February 8, 2013

Thanks to our palliative care physicians, we had a great palliative care MR on pain control at the end of life:
1) Opioid Equivalence:

  • Codeine: 100mg PO
  • Morphine: 10mg PO (5mg IV/SC)
  • Oxycodone: 5mg PO
  • Hydromorphone: 2mg (1mg IV/SC)
2) Opioid Side Effects:
  • N/V: may resolve after a period of time
  • Constipation: does not resolve over time
  • Somnolence/drowsiness
  • pruritis
  • urinary retention
3) Opioid Toxicity:
  • Myoclonus is an early sign of toxicity
  • Nausea/vomitting
  • myosis
  • Somnolence
  • Respiratory depression
4) Treatment of opioid toxicity:
  • Dose reduction 25-50%
  • Change type of opioid
5) Incomplete Cross Tolerance:
  • Results in increased response to an equivalent dose of a different type of opioid
  • Therefore, when changing to a different opioid dose should be reduced by 25-50%

Thursday, February 7, 2013

Post Call Morning Report

This morning we had an interesting discussion on all patients admitted to GIM over night. Here are some interesting topics that were discussed:

1) Treatment arrhythmias associated with cocaine-associated catecholamine excess

  • We discussed a complicated case of an agitated patient with recent cocaine ingestion and atrial fibrillation and signs of heart failure.
  • All types of arrhythmias have been described in cocaine toxicity from wide complex-tachycardia to supraventricular tachycardia
  • Arrhythmias associated with catecholamine excess include SVT, Sinus Tachy, Afib
  • Supportive therapy is the mainstay: cooling, IV fluid rehydration and benzodiazepines
  • Other therapies for SVT/Afib may include IV CCBs 
  • For treatment of HTN may use IV phentolamine/nitroglycerine for HTN (beware of reflex tachycardia)
  • It is important to avoid beta blockers in pts with possible cocaine intoxication as this results in un-opposed alpha and worsening hypertension and coronary vasoconstriction
  • See the following article for more information: Cocaine toxicity and arrhythmias

2) Causes of elevated Lactate

  • Type A lactic acidosis: From marked tissue hypoperfusion: Cardiogenic, septic shock, local decreased perfusion (compartment syndrome, necrotizing fasciitis), ischemic bowel, seizures (from increased O2 use)
  • Type B lactic acidosis: Features of hypoperfusion are not apparent. Causes include toxin-induced impairment of cellular metabolism. causes include: liver failure (from impaired lactic acid utilization in gluconeogenesis in the liver), metformin use in renal failure (theoretical), malignancy (from direct production by malignant cells), cyanide, alcoholism, diabetes.

3) Causes of low BP not responding to fluids

  • In the absence of cardiogenic or septic shock think of more unusual causes of low BP:
    • Anaphylaxis
    • Adrenal insufficiency - mets to adrenals, infarction of adrenals secondary to severe infection (Waterhouse-Friederichsen), hemorrhage/adrenal vein thrombosis, 
    • Hidden bleeding: retroperitoneal

Wednesday, February 6, 2013

Palliative Care Resources

Palliative Care Articles:

This week is palliative care week. Check out the following resources for further reading (Courtesy of Dr. Goche):

Hypertensive Emergency

Today we discussed a patient with a hypertensive emergency. Here are some key points:
1) Classification of HTN:

  • HTNsive urgency: SBP>180 or DBP>120 without end-organ damage 
  • HTNsive emergency: Acute severe hypertension with end organ damage
  • Malignant HTN: Hypertension with papilledema, renal involvement or microangiopathic hemolytic anemia.
2) End organ damage in HTN (head to toe)
  • CNS: Encephalopathy (confusion), seizures, intracranial hemorrhage, SAH, and lacunar infarcts. Radiographic finding called PRES (posterior reversible encephalopathy syndrome) characterized by posterior symmetric white matter edema seen on CT
  • Optic: retinal hemorrhages, exudates, papilledema and vision loss
  • Cardiac: acute MI, aortic dissection, acute heart failure with pulmonary edema
  • Renal: AKI, hypertensive nephrosclerosis (over time)
  • Hematologic: microangiopathic hemolytic anemia
3) HTNsive retinopathy:
  • Mild — Retinal arteriolar narrowing related to vasospasm, arteriolar wall thickening or opacification, and arteriovenous nicking, referred to as nipping
  • Moderate — Hemorrhages, either flame or dot-shaped, cotton-wool spots, hard exudates, and microaneurysms
  • Severe — Some or all of the above, plus optic disc edema. The presence of papilledema mandates rapid lowering of the blood pressure.
4) Secondary causes of HTN: 
  • Endocrine: Cushing's syndrome, pheochromocytoma, aldosterone producing tumour (Conn's syndrome), acromegaly, hyper/hypothyroidism (these do not typically present as emergency/urgency)
  • Anatomic: Coarctation of the aorta
  • Renal: Renal artery stenosis (atherosclerosis, fibromuscular dysplasia), renal parenchymal disease, polycystic kidney disease
  • Drugs: Cocaine, MAOI and tyramine containing foods, rapid withdrawal of clonidine/propanolol
  • Pregnancy: Pre-eclampsia and HELLP syndrome
5) Treatment goals:
  • Hypertensive emergency: Lower the BP by 25% of the MAP in the first 24 hrs or until symptoms resolve (i.e. patient stops seizing)
  • Hypertensive urgency: Safer to lower the BP over days to weeks
6) Practical treatment and specific situations:
  • If HTN emergency consider admission to ICU for arterial line and monitored lowering of BP
  • Labetalol 10mg IV bolus followed by infusion (can repeat bolus if necessary)
  • Nitroprosuside 0.25-0.5mcg/kg/min (beware of cyanide toxicity if prolonged treatment >48hrs)
  • Hydralazine (can cause reflex tachycardia, so better if pt beta blocked prior to starting)
  • Catecholamine driven HTN (Cocaine, MAOI, Pheo): use an alpha blocker (phentolamine 5-10mg IV Q5-15 min). Beware of giving beta-blockers as this can result in unopposed alpha and worsening HTN
  • Pre-eclampsia: labetalol IV and MgSO4
  • Alcohol withdrawal: Benzodiazepines
  • Aortic dissection: Avoid using vasodilators initially (i.e. nitroprusside) as this can cause a reflex tachycardia and sheer stress on the aorta. Start with beta blocker and add nitroprusside if BP still not well controlled.

Tuesday, February 5, 2013

Today Dr. Okrainec led us through an interesting case of an unstable patient. The following are some Clinical Pearls about the management of an acutely ill patient:
1) CAB's & MOIF +/- DONT

  • Circulation: start by assessing the patient's circulation (pulse, BP and HR), feel the extremities to assess for perfusion (cold vs warm). A cool mottled patient is a sign of peripheral vasoconstriction which occurs with hypovolemia or cardiogenic shock. Warm extremities indicate a distributive picture (sepsis or anaphylaxis). If BP low, consider bolusing IV fluids using a pressurized bag, crystalloids have been shown to be equivalent to colloids.
  • Airway/Breathing: Signs of resp distress: tri-poding, paradoxical abdominal breathing (Belly in with inspiration, out with expiration), quiet chest are all indicative of impending resp failure. Also assess GCS for ability to protect the airway. 
  • MOIF: Monitor, Oxygen, IV x 2 and Foley. It is important to ensure the patient is being monitored (i.e. cardiac monitor or nurse at bedside to do frequent vitals). The foley catheter is useful for assessing renal perfusion
2) Primary Survey
  • Once you have assessed the CAB's and initiated initial management (i.e. IV fluids, CPR and ACLS protocol if pulseless) you can do a primary survey
  • The primary survey consists of a quick physical assessment to rule out/in causes of shock:
  • GCS: Pupils (look for a toxidrome), focal neuro deficits, meningismus
  • CVS: JVP (signs of tamponade, HF, PE), new murmurs (acute valvular rupture, aortic dissection)
  • Resp: equal air entry? (signs of pneumothorax)
  • Abdo: signs of perforated viscus, intra-abdo or retroperitoneal bleed (ecchymosis), check the diaper for melena/blood
  • Extrem: signs of DVT
  • Assess around the patient: PCA pump (opiod toxicity)? Heparin drip (bleeding risk)?
3) Initial management:
  • DONT: the universal antitodes for decreased LOC (Dextrose, Oxygen, Naloxone, Thiamine)
  • IV fluids: wide open and on a pressure bag (or use a BP cuff)
  • STAT labs: ABG, CBC, lytes, creat, INR/PTT, lactate, blood C&S, liver enzymes, glucose, troponin/CK. The ABG can tell you roughly the lytes and hgb. Don't forget to look at pt's recent labs
  • STAT investigations based on presentation: ECG, portable CXR, bedside ECHO
  • Low BP resistant to IV fluids: consider giving empiric Abx (early goal directed therapy), consider stress dose of steroids if risk of adrenal insufficiency
  • Low BP resistant to IV fluids: consider giving peripheral inotropic support (phenylephrine 100-200mcg IV bolus, dopamine 10-20mcg/kg/min) can give through peripheral IV for a short period
  • Signs of bleeding: give blood.
4) Definitive management:
  • Call ICU and arrange for transfer once CAB's are relatively stable