Thank you to HH and Katie for co-presenting a case of a young woman with T1DM, CKD presenting with a severe non-anion gap metabolic acidosis with a pH of 7 and a Bicarb of 6! Overall, it was felt that her initial presentation was 2/2 to a mix of GI losses given her profound diarrhea and renal losses of bicarb in early renal dysfunction.
- When calculating the serum anion gap, there’s no need to correct serum sodium for hyperglycemia. The osmotic pull of water would dilute all of the electrolytes in an equal manner, so the sodium, potassium, and chloride are all relatively dilute, and the anion gap calculation would not change.
- When trying to determine where a patient is losing bicarbonate – you can calculate a urine anion gap UAG – see more below.
- In a patient with normally functioning kidneys, they will secrete ketones in their urine. In patients with DKA, this can eventually result in a non-anion gap acidosis.
- Remember risk factors for central pontine demyelination with rapid correction > 10 in 24 hours include: very low sodium levels < 110 (in most cases), premenopausal females and severe malnutrition.
Urine Anion Gap (UAG)
Na + K – Cl = Ur Anion Gap (this is calculating unmeasured anions NH4+ primarily)
- Assumes that the patient is volume replete (Una > 20) and is without an anion gap acidosis
- If UAG + in setting of non-gap metabolic acidosis this suggests the kidneys are FAILING to excrete ammonia à renal tubular acidosis
- If UAG zero or negative, suggests bicarbonate losses from GI tract (this means the kidneys are appropriately getting rid of NH4+ to compensate for acidosis).
- DDx: GI losses (diarrhea or fistulas), early renal failure& ingestions
- These labs must be interpreted in the context of patient’s presentation and there are not strict cut-offs.
- Depending on the severity of the metabolic acidosis, if you have normal kidneys, the urine anion gap should be even more negative (kidney is responding appropriately to excrete NH4+).
- If you have severe metabolic acidosis, and the urine anion gap is zero or only slightly negative, this suggests a mixed picture – in that there are GI losses, but the kidney’s are not responding as robustly as they should to get rid of NH4+. With excretion of NH4+ the CL- amount increases and this should drive the equation above more and more negative.
Non-Gap Acidosis Ddx
- GI losses of HCO3- Diarrhea, fistulas/drainage
- Proximal (Type II): decreased reabsorption & then loss of HCO3-
- Distal (Type I): defect in H+ excretion (hence profound acidosis)
- Hypoaldo (Type IV): acidosis 2/2 to inability to excrete acid
- Early renal failure – impaired generation of NH4+ (this is the KEY to understanding the physiology per above)!
- Ingestions – acetazolamine, sevelamer, toluene
- Dilution – rapid infusion of bicarb free IVFs
- Post-hypocapnia – Rapid correction of respiratory alkalosis -> renal wasting og HCO3 needs to be regenerated
Thank you to Andrew for presenting the case of an elderly man with recent CVA presenting with progressive encephalopathy 2/2 to VZV encephalitis.
- Acute toxic-metabolic encephalopathy (TME) is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease
- Acyclovir neurotoxicity should be considered with new neurological symptoms or encephalopathy 24 hours initiation of treatment, particularly in the presence of renal impairment.
- Herpes zoster encephalitis (HZE) is an uncommon complication of herpes zoster with immunosuppression (HIV, immunosuppressive medications, increasing age) being the principal risk factor for the development of HZE.
- Localized zoster can cause CSF pleocytosis and positive VZV PCR despite lack of active CNS infection -> this is b/c neurons are the primary site of latent virus
- In suspected cases of zoster encephalitis send BOTH VZV PCR and Viral anti-body. The presence of one or both is evidence of small-vessel encephalitis due to VZV.
- VZV encephalitis is rare and life-threatening-> Empirical treatment with IV Acyclovir 10-30 mg/kg per day for 10 days is currently recommended, however no RTCs have been performed.
The figure below outlines the disease pathology of VZV infection from primary infection to reactivation. See Dr. Gilden’s (a leader in the study of VZV) for an excellent review of VZV in the NEJM – “Neurologic Complications of the Reactivation of Varicella-Zoster Virus.”
Thanks you, Arvind, for presenting a case of an older man with exercise-induced bradycardia found to have complete heart block 2/2 to cardiac sarcoidosis.
- In the consideration of bradycardia, one must first rule out MI. 15% of patients with an MI will present with complete heart block.
- Bradycardia in an inferior or posterior MI is driven by 1) ischemia AND 2) the Bezold-Jarisch Reflex. This is a cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle.
- Complete AV dissociation with Ps faster than SLOW QRSs suggests complete heart block.
Etiology of Bradycardia
- Healthy children/adults during sleep (HRs in 30s, pauses up to 2 seconds may occur)
- Well-conditioned athletes
- Some elderly patients
An easy way to break down bradycardia is into extrinsic vs intrinsic causes.
- Idiopathic degenerative d/o
- Ischemia (ACS or chronic)
- Lyme disease
- Viral myocarditis
- Drugs – antiarrhythmics, b-blocker, calcium channel blocker
- Vagal tone
Evaluation of Patient with Complete Heart Block
- Rule out Ischemia – ~15% of patient with an acute MI will have complete heart block (usually RCA)
- Check for systemic, reversible causes of heart block:
- Meds: Digoxin, beta-blockers, calcium channel blockers, or anti-arrhythmics
- Electrolyte abnormalities – hypokalemia
3. Look for the primary cardiac causes in 3 broad categories:
- Infiltrative: Amyloidosis, hemochromatosis, sarcoidosis
- Inflammatory: SLE, scleroderma
- Infectious: Rheumatic fever, Chagas, endocarditis, viral myocarditis,i syphilis, Lyme disease
Diagnostic Criteria for Cardiac Sarcoid
Here is a great JACC review on cardiac Sarcoidosis – http://www.onlinejacc.org/content/68/4/411
Thank you to Ashley S.M. for presenting a really fascinating case from the ICU. We talked about a middle aged man with HIV/AIDS off ARVS, who presented with DOE, found to have multiple atrial masses and tamponade, ultimately d/t an infiltrative cardiac lymphoma (path pending).
We talked about this case at two reports, so here are the combo of learning points!
Approach to Atrial Masses
Masses in the heart can have hemodynamically significant effects on circulation, valve function, and risk for embolization.
Ask yourself 1) is this a real mass or is it actually just a clot? 2) if a mass, is it benign or malignant? 3) for malignant masses, consider both primary neoplasm and metastatic disease. Overall, the most common cause of an atrial mass is a benign atrial myxoma. See the attached table below, but important malignant causes to consider are sarcoma, lymphoma and metastatic tumors. Given his HIV/AIDS, our infectious differential also included
- Infective endocarditis with large valvular veg or very large perivalvular abscess
- TB endocarditis (usually more pericardial involvement)
- Endemic fungal disease: especially in CA, consider cocci for cardiac involvement
HIV associated malignancies: Monica Gandhi helped share a useful framework about thinking about the three main oncogenic viruses that cause malignancy in pts with HIV. For all of these malignancies, also critically important to start ARVs right away!
- Cervical / anal / head and neck squamous cell cancers: HIV infected patients are less able to clear oncogenic strains of HPV. The incidence of cervical dyplasia (CIN) in patients with HIV is 4-5x higher than in patients without HIV.
- EBV : highly associated with Burkitt’s and DLBLC. Remember that these lymphomas can be exquisitiely responsive to chemotherapy so it is important to start treatment right away.
- Kaposis Sarcoma
- Castlemans disease (multicentric form)
- Primary Effusion Lymphoma
Burke A, Jeudy J, Virmani R. Cardiac tumours: an update. Heart 2008;94:117-123. http://heart.bmj.com/content/heartjnl/94/1/117.full.pdf
Thanks to Gladys for presenting a fascinating case of a 40F with HIV who presents with fever, oral ulcers found to have retroperitoneal lymphadenopathy and ultimately diagnosed with disseminated histoplasmosis.
1.The most common causes of oral ulcers are aphthous ulcers and HSV infection. A second pass work up includes investigation for a wide variety of infectious, autoimmune, malignancy, drug-induced or autoimmune blistering conditions.
2. Granulomas are caused by a wide variety of infectious, autoimmune, malignant processes. Immunodeficiency [e.g., chronic granulomatous disease] and foreign bodies [e.g, TALC granulomatosis] are other considerations. Owing to their morbidity and the possible need for immunsuppression/chemotherapy if a autoimmune or malignant cause is found, an initial focus on infections [usually intracellular bugs] is important.
3. Unlike the other endemic mycoses, histoplasmosis is an intracellular organism [lives in macrophages]This changes the clinical behavior and unlike the other endemic mycoses involves the liver, spleen, bone marrow, GI tract [oral ulcers and ileitis], and adrenal glands.
- The most common causes of oral ulcers are aphthous ulcers and HSV infection. A second pass work up includes investigation for a wide variety of infectious, autoimmune, malignancy, drug-induced or autoimmune blistering conditions.
- Here is one approach.
- Granulomas are caused by a wide variety of infectious, autoimmune, and malignant processes. Immunodeficiency [e.g., chronic granulomatous disease] and foreign bodies [e.g, TALC granulomatosis] are other considerations.
- Owing to their morbidity and the subsequent need for immunsuppression/chemotherapy if a autoimmune or malignant cause is found, an initial focus on infectious causes [usually intracellular bugs] is important.
- Epidemiology: worldwide distribution
- Incubation period: 1-3 weeks
- Asymptomatic burden: Like the other endemic mycoses, there is a high rate of asymptomatic disease [around 80% without symptoms]
- Unlike the other endemic mycoses, histoplasmosis is an intracellular organism [lives in macrophages]
- This changes the clinical behavior and unlike the other endemic mycoses involves:
- Liver, spleen, lymph node and bone marrow involvement
- GI tract
- Oral mucosa and ileum are the most common sites of involvement.
- Adrenal glands [similar to Tb involvement]
- Also results in this being hardest to diagnose [like Tb]
- Clinical Symptoms:
- Occur as primary infection or reactivation disease in immunosuppressed hosts
- Pulmonary Symptoms – most common
- Acute or subacute flu like illness occur
- Minority have fulminant pulmonary disease
- Reticulonodular (with effusion) most common
- Erytema nodosum may accompany pulmonary disease
- Extra-Pulmonary disease
- Who? —> immunosuppressed
- Reticuloendothelial system: liver, spleen, lymph nodes, bone marrow
- GI tract
- Like Crohn’s anywhere along the GI tract
- Oral mucosa and ileum most common
- Fibrosing mediastinitis
- Constrictive pericarditis
- A sepsis-like syndrome in AIDS patients
- Of the mycoses this is the hardest to diagnose, because antigen based testing + culture have lower sensitivity [ possibly due to the intracellular nature of the organism]
- Culture: 75% [vs >in other mycoses]
- Urine antigen: Sen, Spec 70%
- Sen, Spec 90%
- Cross-reactivity with blasto
- Mild disease: none
- Moderate: Intraconazole
- Severe: Ampho
Thank you to Dr. Wolters for joining us today and to Tyler for presenting the case of a man w/ hx of SCC on pembrolizumab p/w 2 months of DOE & 1 wk of cough not responsive to levofloxacin. We discussed the role of ABGs > VBGs and the ddx for organizing PNA. The patient ended up having pneumonitis 2/2 to his PD-1 inhibitor which was discontinued and he was then started on steroids.
- There are several toxicities associated with PD-1 inhibitors. See here for prior pearls on these check point inhibitors!
- One needs to lose ~ 50% of their lung function to have SOB @ rest!!
- Try to obtain an ABG in a patient who is hypercarbic given the variability of a VBG and its estimation of pCO2. Per Dr. Wolter’s the pCO2 from a VBG can be wrong ~ 20% of the time.
- Reverse Halo Sign (RHS) on a CT Chest is a patch of normal lung surrounded by abnormal densities . There is a ddx and figure for RHS below!
ABG vs. VBG – Thank you Kenny for sharing!!
- Arterial: accurate O2 content; nl pH = 7.4 (7.35-7.45), CO2 = 40 (35-45)
- Venous: carries excess CO2 to be ventilated off in the long. ~3-5 mmHg higher than arterial blood
Evidence: Systemic review and meta analysis
- Arterial pH ~ 0.03 higher than venous
- Venous and arterial pCO2 do NOT correlate that well (off in ~ 20% of gases)
- Good negative predictive value of CO2 if low, but not as helpful if high
- If you want O2 status, you can use SpO2 as a surrogate marker, but ABG is more accurate
- If concerned for pH or CO2 status and ABG isn’t easy (ie painful and technically challenging); VBG as 1st pass -> understand limitations
- If the VBG doesn’t make sense or you want to be totally sure, get an ABG
Defined as the lung’s response and subsequent repair to any insult. Often associated with the reverse halo sign (RHS) characterized by a central clearing surrounded by denser air-space consolidation (often ground glass) in the shape of ring/crescent. This happens because in the following situations the lung heals from the center outwards. Was initially described in cryptogenic organizing PNA, however is now part of a wider DDX that includes the following:
- Autoimmune (Sarcoid, Wegener’s granulomatosis)
- Drug effect – PD-1 Inhibitors à 5% of patient’s will develop pneumonitis @ a mean of 7 months; 85% will respond to discontinuation & steroids.
- Infectious – endemic fungal infections, PCP PNA,
- Idiopathic – cryptogenic
Here is a great article and figure on the evaluation of Revere Halo Sign (RHS)
Thank you so much to Julia Janssen for presenting the case of an elderly woman with a history of HFpEF, OSA, pHTN who was admitted for shortness of breath. In talking through this case, we had the opportunity to review the concept of caring for geriatric patients.
Inpatient Care for Geriatric Patients:
- Remember that geriatric patients are a vulnerable population that likely need additional attention in the hospital
- Remember that functional status has been repeatedly demonstrated to be a predictor of mortality, 30-day readmission, and readmission over a much longer period of time
Geriatric History and ROS:
Here are a few highlights to consider when taking a medication history:
- especially ask about high-risk meds (benzos, opiates, anti-psychotics, anticoagulants, cardiac meds). Consider consulting the Beers list (Click here for PDF)
- utilize team pharmacist to help with a thorough med rec (look at bottles, call pharmacy, etc)
- Social History:
- Social support – loneliness in the elderly is a serious problem that has been linked to worse outcomes
- Who lives at home with you? Who would you call in case of an emergency?
- Geriatric ROS: This is somewhat of a comprehensive list, but something to consider
- ADLs (Eating, Bathing, Dressing, Toileting, Transferring):
- IADLs (Medications, Laundry, Housecleaning, Telephone Use, Groceries, Bills)
- Mobility: How many flights of stairs can you go up?
- Falls: How many falls have you had in the last week, month, year?
- Depression: Are you feels sad, down, depressed? Have you lost interest in things that used to make you happy?
- Hearing/Visual Impairment: Do you have any problem with your hearing or vision?
- DME: Do you have or use any assistive devices?
- Cognitive Impairment: Have you noticed any changes in your memory? Do you ever find yourself lost or not recognizing people you should know?
- Driving Status: How many accidents have you been in in the last year?
- Elder Abuse: Do you ever feel threatened or unsafe at home?
- Incontinence: Do you have have issues leaking urine or stool?
- Constipation: Do you ever have any issues with constipation
- Advanced Directives
- A MUST, MUST, MUST
- If nothing has been done, and you want to provide resources for your patient:
- Additional Resources for Preparing for Advance Care Planning can be found on the following websites: