Category Archives: Morning Report

Morning Report

Lymphocytic hypophysitis – 10/3/18

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Thanks to Sahar for presenting the interesting case of a middle-aged woman with metastatic melanoma recently started on ipilimumab who presented with a headache and fatigue, found to have hypothyroidism and adrenal insufficiency with work up consistent with hypopituitarism related to an adverse effect of ipilimumab: lymphocytic hypophysitis!

Clinical Pearls

  • Remember that adrenal insufficiency and hypothyroidism are causes of elevated ADH levels.
  • Red flags for obtaining head imaging for headache include age >55, sudden onset, positional, onset after trauma or exercise, fever, focal neuro findings, and immunosuppression.
  • Pituitary adenomas can have three manifestations: mass effect, hormonal hypersecretion, and hypopituitarism.  When imaging shows a pituitary mass, your work up should address each of these categories.
  • The most sensitive test to assess hypothalamic-pituitary access function is LH/FSH!
  • Immunotherapies are commonly associated with a flare of autoimmune diseases.  A more rare side effect of CTLA-4 inhibitors (like ipilimumab) is lymphocytic hypophysitis (inflammation of the pituitary gland)
    • This condition commonly presents with headache out of proportion to neurologic findings and preferential decline in ACTH and TSH though other hormones can also be impacted.
  • For hypopituitarism, remember to always treat adrenal insufficiency first before replacing thyroid hormone.  Failure to do so can precipitate adrenal crisis!

Indications for imaging a patient with headache:

  • Age >55
  • Sudden onset
  • Worse with lying down or wakes patient from sleep
  • Rapid onset after trauma or exercise
  • Fever
  • Focal neurologic findings
  • New headache in immunosuppressed patient

Pituitary adenoma:

  • Evaluate for the following
    • Mass effect: visual field deficit, headache
    • Hormonal hypersecretion
      • Prolactin ⇒ galactorrhea, amenorrhea, infertility
      • GH ⇒ Acromegaly
      • TSH ⇒ hyperthyroidism
      • ACTH ⇒ Cushing disease
      • ADH ⇒ SIADH
    • Hyposecretion:

Capture

Hypophysitis:

  • Inflammation of the pituitary
  • Four categories based on histologic findings:
    • Lymphocytic
      • Most common form
      • Seen in late pregnancy and post-partum period
      • Also associated with ipilimumab as our patient here!
    • Granulomatous
      • Idiopathic or secondary to GPA, sarcoid, TB
    • Plasmacytic (IgG4-related)
    • Xanthomatous (most rare)
  • Clinical presentation
    • Headache out of proportion to exam findings
    • Preferential decrease in ACTH and TSH ⇒ adrenal insufficiency and hypothyroidism
  • Prognosis:
    • Pituitary size eventually normalizes but pituitary loss of function is often permanent.

Hyponatremia:

Lastly, refer to this algorithm from our recent morning report to help you think through hyponatremia.

Morning Report

Acute pancreatitis – 10/2/18

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Thanks to Tiffany for presenting the case of a middle-aged man presenting with acute onset of epigastric abdominal pain and nausea/vomiting, found to have a normal lipase initially which jumped up to 1150 48 hours later consistent with acute pancreatitis.

Clinical Pearls

  • Gallstones and ETOH account for the majority of cases of acute pancreatitis.
  • Up to 30% of cases of acute pancreatitis are idiopathic!  This is a diagnosis of exclusion.
  • Lipase typically rises within 4-8 hours after the onset of pancreatitis and lasts for >8 days as opposed to amylase (6-12 hours, lasts for 3-5 days).  Lipase is also more sensitive and specific than amylase.
  • Common electrolyte abnormalities associated with pancreatitis are hyperglycemia and hypocalcemia.
  • BISAP, Ranson’s, and APACHE II scores are useful for prognostication
  • In a patient with history of recurrent pancreatitis presenting with acute GI bleed, think hemosuccus pancreaticus (pseudoaneurysm between the splenic artery and pancreatic duct) which requires IR or surgical intervention.

Causes of pancreatitis: GET SMASHED

  • Gallstones
  • EtOH
  • Trauma
  • Scorpion bite (and Gila monster!)
  • Mumps, Malignancy (pancreatic adenocarcinoma)
  • Autoimmune (seen in IgG4 related disease and celiac)
  • Steroids
  • Hypertriglyceridemia and Hypercalcemia (unclear mechanism)
  • ERCP
  • Drugs (sulfas, thiazides, ACEi, lasix, ARVs are most common)

If you have ruled out the above etiologies, here is a more thorough list to sift through:

  • Infections
    • Viruses: coxsackie, CMV, HIV, VZV, HBV, HSV
    • Bacteria: salmonella, legionella, mycoplasma, leptospira
    • Fungi: aspergillus
    • Parasites: toxo, crypto, ascaris
  • Hypotension
  • Atheroembolism
  • Vasculitis (SLE or PAN)
  • Hereditary mutations
  • Cystic fibrosis

Work up for pancreatitis without identifiable cause:

  • EUS with bile sampling for microlithiasis
  • If EUS is negative or unavailable, then MRCP with secretin administration to evaluate dynamic obstruction or early chronic pancreatitis

Prognosis:

Capture

For a very thorough review of pancreatitis, please see this prior blog post.

Morning Report

GPA – 10/1/18

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Yours truly presented a case of a middle-aged woman with a recent history of otitis, sore throat, conjunctivitis, photophobia, and arthralgias who presented with chronic and progressive decline in functional status and AMS, found to be uremic with work up revealing c-ANCA associated ESRD.

Clinical Pearls

  • Remember that oval fat bodies are specific for glomerular pathology (more commonly nephrotic syndrome but can be seen in nephritic disease as well).
  • ANCA-associated vasculitides include GPA, MPA, eGPA (and renal-limited vasculitis).
  • All have similar features on renal histology (focal necrotizing, crescentic, pauci-immune glomerulonephritis).
  • They can affect multiple organ systems (see breakdown below) which makes their clinical diagnosis challenging apart from the following differences:
    • c-ANCA is associated with GPA, p-ANCA is seen in MPA and eGPA
    • Granulomas are seen in GPA and eGPA
    • Eosinophilia and asthma are associated with eGPA

ANCA-associated vasculitides

Capture

Chart above adapted from this paper by Koldingsnes et al.

Granulomatosis with polyangiitis (GPA)

Diagnostic criteria (two or more has 88% sensitivity and 92% specificity):

  • Nasal or oral inflammation (painful/painless oral ulcers, or purulent or bloody nasal discharge)
  • Abnormal chest radiograph showing nodules, fixed infiltrates, or cavities
  • Abnormal urinary sediment (microscopic hematuria w/w/o red cell casts)
  • Granulomatous inflammation on bx of artery or perivascular area

Clinical presentation:

  • Most commonly in older adults, M=F
  • More common among white individuals (~89%)
  • S/s
    • Fatigue, fever, weight loss, arthralgias, rhinosinusitis, cough, dyspnea, urinary abnormalities, purpura, and neurologic dysfunction.
    • ENT
      • 90% of GPA cases, only 35% of MPA
      • Nasal crusting, sinusitis, otitis media, earache, polychondritis, ulcers, discharge
      • Conductive and/or sensorineural hearing loss
      • Saddle nose deformity
    • Tracheal and pulmonary disease
      • Airways or parenchyma
    • Renal
      • ~18% at presentation but subsequently develops in 77-85% of patients within the first 2 years of disease onset
      • High risk of progression to ESRD
      • Asymptomatic hematuria
      • Subnephrotic range proteinuria
      • Rapidly progressive GN
    • Cutaneous
      • ~50% of patients
      • Leukocytoclastic angiitis is most common which causes purpura of lower extremities
      • Other findings: urticarial, livedo reticularis, nodules, erythema nodosum, pyoderma gangrenosum, and Sweet syndrome
    • Ophthalmic/orbital
      • Conjunctivitis, corneal ulcers, episcleritis/scleritis, optic neuropathy, retinal vasculitis, and uveitis.
    • Other organs
      • CNS: neuropathy, CN abnormalities, mass lesions, hearing loss, granulomatous inflammation of the CNS
      • GI tract, heart, lower GU, parotids, thyroid, liver, or breast
      • High incidence of DVT (unclear mechanism)
    • Can progress slowly over months or explosively over days
    • Relapses can manifest differently than original presentation

Diagnosis requires biopsy!

Treatment:

  • Prompt initiation of therapy can be life and organ sparing
  • Induction therapy: Steroids +-Cyclophosphamide +-Rituximab
  • Maintenance therapy: multiple options-Azathioprine, MTX, Rituximab, Leflunomide
Morning Report

Wound botulism – 9/26/18

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Thanks to Alison for presenting the case of a middle aged man who presented with acute onset of ptosis, dysphagia, and dysarthria, with an evolving exam found to have botulism secondary to IV injection of black tar heroin.

Clinical Pearls

  • Botulism is extremely rare! Only 110 cases were reported last year in the US with 70-75% of them being related to infant botulism, 20-25% foodborne, and 5-10% wound botulism.  The latter category has been on the rise especially in California.
  • Most common form of botulism is infant botulism
  • Botulism presents with bulbar symptoms; progressive, descending paralysis; absent reflexes; and autonomic dysfunction
  • Management involves the following
    • Notify the Department of Public Health ASAP if botulism is on your ddx
    • Obtain wound/blood cultures (special tube to be sent to DPH)
    • Administer antitoxin EARLY (do NOT wait for culture confirmation)

Capture

For more information, check this prior post on our blog.

Morning Report

Ophthalmoplegic migraine – 9/25/18

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Thanks to Joe fore presenting the case of a middle aged woman with a history of migraines who presented with acute onset of painless binocular diplopia, found to have an isolated CN3 palsy concerning for ophthalmoplegic migraine after an extensive work up.

Clinical Pearls:

  • Types of diplopia:
    • Binocular diplopia refers to diplopia that is only present when both eyes are open (goes away when one eye is closed) and results from ocular misalignment.
    • Monocular diplopia refers to diplopia that is present even when one eye is closed and is more consistent with a local eye disease (globe related processes involving the cornea or the lens).
  • Approach to diplopia is similar to any neurologic deficit in which you would localize the lesion!
    • Upper motor neuron (brain)
    • Peripheral nerve (cranial nerves)
    • Neuromuscular junction
    • Muscle (extra-ocular muscles)
    • Globe (local eye disease or refractive error)
  • CN3 palsy usually presents with the eye in the “down and out” position and can also impact the levator palpebrae muscle resulting in ptosis.  These result from ischemia at the center of the nerve (secondary to diabetes/HTN).
    • In a patient with CN3 and a dilated pupil, you must rule out a PCA aneurysm!  Impingement of the CN3 by an enlarging aneurysm cuts off the parasympathetic fibers running on the outside of the nerve, resulting in a dilated pupil.  This is the only aneurysm that gives a warning sign before rupture!

Commonly tested gaze palsies:

Capture

Ophthalmoplegic migraine:

  • Rare condition, often manifests in children and young adults
  • Diagnosis of exclusion
  • Most commonly affects CN3 (but can go to CN4 and CN6 as well)
  • Can sometimes precede the headache
  • Permanent nerve damage has been reported and some believe that it is a demyelinating neuropathy (for more info, refer to this review article)

 

 

Morning Report

Acute Epiglottitis 9/24/2018

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Yves-Paul presented a case of a middle age man with poorly controlled diabetes presenting with acute onset sore throat, which quickly progressed to dyspnea and dysphagia. He was noted to have stridor on evaluation and he was urgently intubated for airway protection. Subsequent endoscopic exam revealed a grossly purulent and inflamed epiglottis consistent with an abscess.

Stridor vs Wheezing

  • Stridor: Upper airway, inspiration, single pitch (remember the sound quiz we did?)
  • Wheezing: Relatively lower airway, expiratory musical sounds, but in bad cases can see wheezing in both

Picture1

Epiglottitis

Epidemiology

  • Kids more common (H. influenzae type B) but less common now due to vaccination.

Risk Factors

  • Kids: Immune deficiency, incomplete immunization
  • Adults: Immune deficiency, diabetes

Presentation: Drooling, dysphagia + odynophagia, dyspnea/distress

  • Acute in adults over 24-48 hours Kids can be hyperacute (< 12 hours) leading to airway compromise.
  • Obstruction less acute in adults due to larger AW diameter
  • Sore throat and odynophagia in most cases
  • Fewer have airway compromise; signs to look for are:
    • Drooling
    • Muffled voice
    • Respiratory distress
    • Stridor (impending obstruction)
    • Tripoding, extended neck (maximizes airway diameter)

Diagnosis:

  • Lateral X-ray with thumb sign demonstrates an enlarged epiglottis.

Picture2

  • Direct visualization (fiber optic), beefy red, stiff, edematous epiglottis is diagnostic.

Picture3

As you can see, the surrounding structures were grossly edematous and inflamed to the point we cannot identify the vocal cords at all.

Pathophysiology

  • Organisms: Strep, staph, non-type H.influenzae, beta hemolytic strep, Klebsiella
  • Viral: HSV, EBV, Para/influenza, VZV
  • Non-infectious: Foreign body

Management:

  • Secure airway FIRST. No not manipulate or remotely touch. Can be nasotracheal or orotracheal. If unable to intubate, tracheostomy can be done.
  • Abx: Beta lactamase resistant class (usually 3rd gen cephalosporin) in general unless also suspecting staph/strep, then add vancomycin as well
  • I&D if abscess

Picture4

 

Morning Report

Elevated Alk Phos… Only Clue to Breast Cancer 9/20/2018

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Sarah presented a middle age woman with a history of schizophrenia, HFpEF, possibly COPD, who presented from her Board and Care facility due to inability to ambulate. She was able to provide much of a history but her exam was normal. Her labs were notable for alk phos in the 700-1000 range, and mildly elevated AST/ALT in the 60-70s. An abdominal US revealed hepatic steatosis but really nothing else… Her medical history was also obscure since she receives her care from multiple institutions.

She was incidentally found to have a breast mass on exam, and subsequent work up for her elevated alk phos unfortunately revealed metastatic breast cancer.

Elevated Alk Phos

Background: Alk Phos is derived from mainly bone and liver, higher in men, varies with age (higher in kids, thought to be due to physiologic osteoblastic activity)

GGT (gamma glutamyl transpeptidase): liver specific, can be used to verify if alk phos elevation is due to biliary disease if GGT is also elevated.

Alk Phos

Breast Cancer

Most common tumor in women

Risk

  • > 50
  • Personal Hx
  • Strong family Hx of pre-menopausal breast cancer
  • Genetic BRCA 1 & 21
  • Personal hx or ovarian or endometrial cancer
  • Dense breasts
  • OCP use for > 15 years
  • Late menopause

Screening:

  • Screen F > 50 or < 5-10 yrs prior to age in 1st degree relative with breast cancer, and then Q2yr
  • More frequent screening recommended for specific mutations, i.e. BRCA, TP53, then MRI Q year
  • How about F with breast implants? MRI, CT, or mammogram? The recommendation is still mammogram but with multiple views

 

Common Scenarios:

Breast

Local disease in situ No malignancy beyond basement membrane Lumpectomy + RT, or mastectomy. If ER +, use tamoxifen/aromatase inhibitors
Lobular carcinoma in situ (LCIS) Isolated to lobule, within basement membrane, not exactly cancer yet but high risk ER+ use tamoxifen/AI to dec risk of development into invasive breast cancer.

NSABP-P1 trial: Pt with LCIS tx with tamoxifen dec risk of invasive breast cancer, but inc risk of endometrial cancer esp in > 50yo
Infiltrating ductal carcinoma, LN negative Spread beyond BM, need to sample sentinel LN, if negative, no further need for dissection. Wide excision of mass with free margins + RT, adjuvant chemo for size > 1cm. Tamoxifen/AI if ER +
Infiltrating ductal carcinoma with LN positive Same as above but LN +, warrants further LN dissection, automatic adjuvant chemo Wide excision (modified radical mastectomy), RT + adjuvant chemo + Tamoxifen/AI if ER+.
Local invasive dz involving skin or chest wall   Chemo followed by mastectomy, + tamox/AI if ER+

Lymph node positivity is the most important prognostic factor, followed by tumor size, then receptors, and then grade.

For diagnosis, always get excision biopsy for dx, FNA has low sensitivity, hence even if negative, always follow by excisional bx.

Receptors and Management

  ER+ ER- HERR2+
Pre-menopausal Chemo + tamoxifen Chemo + trastuzumab
Post-menopausal Aromatase inhibitors + chemo Chemo + trastuzumab

Tamoxifen: Use for 10 years if ER/PR+. Dec risk of new breast cancer and effective for metastatic dz of receptor positive.

Down side: inc risk of endometrial cancer 3x, inc thromboembolic risk.

Aromatase inhibitors: Watch out for osteoporosis

Morning Report

92% blasts… Fever… AND a rash?! 9/19/2018

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Narges presented a case of a middle age woman without any prior medical history, presenting with 1 week of bruising, epistaxis, and bleeding from her gums. Her initial lab work was notable for a WBC of 52.2 with 92% blasts, later confirmed to be AML. She developed a fever and a rash over the next few days… She had neutropenic fever, and around the same, time, developed AML-associated Sweet’s Syndrome!

AML: A quick overview

Accounts for 80% of acute leukemias in adults

Risk Factors

  • Benzene exposure
  • Radiation exposure, commonly 7-10 years after exposure
  • Prior tx with alkylating agents and topoisomerase II inhibitors like doxorubicin, etoposide.
  • Age: greatest risk factor, older = at high risk, median age 65
  • CML, MDS, and myeloproliferative syndromes have a chance to evolve into AML.

Initial presentation

  • Bruising, gum bleeding, epistaxis from thrombocytopenia
  • SOB, DOE, fatigue from anemia
  • Pyogenic infections of the skin
  • HSM found in 1/3 of pts
  • 50% might have gingival hyperplasia as first signs of the disease
  • Small subset might have concurrent HLH on presentation
  • If fever, almost always infection

Diagnosis

  • Buzz words: blasts on smears, Auer rods (peroxidase stain)
  • > 20% blasts cells
  • Flow cytometry
    • CD117, CD33 most common
    • CD19, if seen, suggests lymphoblastic origins
  • Subtypes
    • M3 (Acute promyelocytic leukemia), t(15; 17), prone to DIC, responsive to ATRA and potentially can be cured.
      • If pt receiving ATRA +/- Arsenic trioxide develop pulmonary sx think of an entity called Differentiation Syndrome, can be life threatening, stop treatment and give steroids.
    • Non APL: Everything else

Management:

  • Induction, consolidation (after complete remission, assess induction response via BM bx) via HiDAC high dose cytarabine, or autologous CT, or allogeneic HCT, maintenance (usually not needed but can be beneficial in some types of AML)
  • APL: ATRA +/- ATO
  • Non-APL: 7 day course of cytarabine and 3 day course of an anthracycline. For older pts with more comorbidities, can use a milder regimen with azacytidine or decitabine.

 

Neutropenic fever

Definition: T > 38.3 or > 38 sustained over 1 hour, with neutropenia (ANC < 500)

Determine high risk or low risk

  • Low Risk: Anticipated neutropenia < 7 days, clinically stable, NO medical comorbidities
    • IDSA: Can consider outpatient antibiotics, Cipro + Augmentin and able to tolerate PO, otherwise inpatient management
  • High Risk: Anticipated neutropenia > 7 days, clinically unstable, any medical comorbidities
    • Automatically inpatient management
    • Monotherapy with pseudomonal coverage initially is recommended by IDSA
      • Cefepime: 2g Q8H, higher dose than usual
      • Meropenem 1g Q8H
      • Imipenem
      • Zosyn 4.5g Q6-8
      • Ceftazidime increasingly avoided.
    • If history of MRSA, e/o catheter infection, skin infection, pneumonia, or unstable, add Vancomycin/MRSA coverage
    • PCN allergy: Can consider using Aztreonam, cipro
    • If recurrent of persistent fever after 4-7 days: Add an empiric antifungal, most of the time cover for candida since it’s the most common cause of invasive fungal infection.
      • Echinocandin is favored i.e. caspofungin, increasing azole resistance in candida.
      • Think aspergillus if e/o pulmonary nodules, ampho B and voriconazole then are preferred

Sweet’s Syndrome

Uncommon, inflammatory disorder, usually affects pts ages 30-60. Older = more likely malignancy associated

Presentation:

  • Abrupt, painful, edematous (juicy), erythematous papules/plaques/nodules + fever and leukocytosis.
  • Rare mucosal/oral involvement.
  • Can also rarely causes inflammation of a particular organ system, i.e eye, liver, heart, CNS, kidney, even bone.

Sweet.jpgImage adapted from Derm 101

Types

  • Classic
    • Idiopathic, majority of cases
    • Associations: Infections (URI, GI) 1-3 weeks after infection
    • IBD
    • Pregnancy
    • HIV, TB, hepatitis, autoimmune conditions
    • Possible inc risk of malignancy
  • Malignancy associated
    • AML is the malignancy most associated with Sweet’s Syndrome.
    • Risk:
  • Drug-induced (long list but some of the potential ones we used more commonly are):
    • Bactrim, Macrobid, AED, hydralazine, clozapine, PTU, GCSF, Mirena, Lasix, Azathioprine, ATRA

Dx Criteria: both majors and 2 minors are required

  • Majors
    • Abrupt onset of painful erythematous plaques or nodules
    • Histopath evidence of dense neutrophilic infiltrate without evidence of leukocytoclastic vasculitis
  • Minor:
    • > 38C
    • Underlying malignancy, IBD, pregnancy, or recent upper resp, GI infection, or vaccination
    • Steroid responsive
    • Labs: ESR > 20, CRP elevated, leukocytosis > 8000 with > 70% neutrophils)

Biopsy: Dense, neutrophilic infiltrate in the dermis, w/o e/o vasculitis.

Morning Report

Hyponatremia – 9/18/18

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Thanks to Joe for presenting the case of a young man with no known medical history who presented with acute onset of generalized weakness, found to have symptomatic hyponatremia to 120 resulting from psychogenic polydipsia!

Clinical Pearls

  • Hyponatremia is largely a problem of too much free water (sometimes compounded by too little solute) and defined as a Na <135
  • Pick a systematic approach to solving the underlying diagnosis for any patient with hyponatremia (see below for one possible outline).
  • The term “pseudohyponatremia” refers to the presence of substances that interfere with laboratory measurement of sodium concentration in the blood, specifically high triglycerides and paraproteins.
    • Hyperglycemia does NOT fall into this category because glucose is osmotically active and pulls water into the intravascular space, resulting in a dilutional and true hyponatremia.
  • Chronic hyponatremia (>72 hours) must be corrected slowly to avoid osmotic demyelinating syndrome (ODS).  Acute hyponatremia (<48 hours) can be corrected more rapidly.  That said, we rarely have a Na value within 48 hours prior to patient presentation to determine acuity.  As a result, and given the neurologic risks, most patients are treated as if they have chronic hyponatremia.
  • ADH leads to increased uric acid excretion through the kidneys so low serum uric acid levels have been associated with SIADH.  But this test is not very specific.
  • Osmolarity of normal saline is 308 compared to human serum which is normally 280-295.  In a hyponatremic patient, NS infusion becomes a relatively hypertonic (rather than isotonic) solution!

Schematic

For more detailed information, refer to this prior post and this review article.

Morning Report

Metformin Associated Lactic Acidosis (MALA) 9/17/2018

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Thanks to doctor-in-training Emma who presented a case of an elderly woman, on dialysis, who came in with SEVERE lactic acidosis due to a variety of factors, but largely contributed by being prescribed metformin 2 weeks prior to presentation.

We will use this case to illustrate several concepts:

On initial presentation, pt was in a state of shock. If you remember from medical school, there are mainly 4 types:

  • Cardiogenic
    • Myopathic (DCM, acute MI)
    • Mechanical (Acute MR, VSD, severe AS)
    • Arrhythmia
  • Hypovolemic
    • Hemorrhage, volume depletion
  • Distributive
    • Sepsis
    • Anaphylaxis
    • Neurogenic (spinal cord injury)
    • Endocrine (myxedema, Addison’s)
  • Obstructive
    • Pericardial tamponade
    • PE
    • Pneumothorax

Shock can also be approached from a cardiac output standpoint to help differentiate the potential causes:

Capture

If someone is hypovolemic, but he/she is found to be hypotensive but bradycardic (instead of tachycardic), remember from physiology:

MAP = CO x SVR, where CO is cardiac output, SVR is systemic vascular resistance

CO = SV x HR, SV is stroke volume, and HR is heart rate.

Hence in a state of hypovolemia, the body will attempt to maximize CO by increasing HR to maintain adequate MAP. If you see the opposite though, there could be something else going on…

  • Cardiac: MI, conduction abnormalities, infectious (Lyme, Charga’s)
  • Toxic/Meds: CCB, Beta blocker, Dig, Alpha 2, organophosphate
  • Lytes: Hyperkalemia -> heart block -> sinus arrest
  • Endocrine: Hypothyroidism (myxema coma), adrenal insufficiency
  • Environmental: Hypothermia
  • Neurogenic shock

 

Acid-Base: Acid-base disorders can appear daunting, but the following algorithm can make things simpler if followed consistently. We will work through this patient’s acid/base disorder together. Her HCO3 is 6, AG of 52, with an ABG of 6.83/13/170.

  1. Look at the pH: < 7.4 automatically means some sort of acidosis is going on.
  2. Next look at the PCO2, if it is in the same direction as the pH (low PCO2 in this case, and low pH), then it is suggestive of a primary metabolic rather than a respiratory issue causing the acidosis. If pH is low and PCO2 is high, then there is high suspicions for a respiratory process driving the acidosis.
  3. Look at the Anion Gap, which in this case in 52. Go through your differential for AGMA.
  4. Calculate the Delta Gap. This basically is a way to assess whether a mix acid/base disorder exists after taking into account the AG. To help illustrate:Capture2
  5. Delta gap = calculated AG – normal AG = 52 – 12 = 40. Now there are several ways to do this, but one method that’s quick and simple is to simply add this delta gap to the measured bicarb and see what other metabolic acid/base disorders can be hiding beneath the anion gap. In this case, 40 + 6 = 46, which is suggestive of an underlying metabolic alkalosis.
  6. Lastly, calculate compensation. For AGMA, use Winter’s Formula = 1.5 (HCO3) + 8 +/-2. The calculated PCO2 should be 15-19. Since our measured PCO2 is 13, which is lower than expected, then this is suggestive of an underlying respiratory alkalosis as well, probably due to sepsis.
  7. Our final answer for the acid/base disorder for this patient is: AGMA with metabolic alkalosis and concurrent respiratory alkalosis!

 

Lactic Acidosis: Traditionally we view this as a sign of sepsis, or a marker of tissue hypoperfusion. However this is not always the case!

  • Type A: Inadequate oxygen delivery
    • Rule of thumb: Tissue hypoperfusion, tissue ischemia
    • Can also be seen with increased anaerobic muscular activity, like generalized convulsions in a seizure
    • Can also be seen in hypoxemia, severe anemia
    • Cryptic shock (elevated lactate, okay BP), similar to overt septic shock in terms of mortality in setting of severe sepsis.
  • Type B: altered physiology, others
    • B1: Underlying disease, malignancy, hepatic & renal failure
    • B2: Drugs, toxins
    • B3: Inborn errors of metabolism, enzyme deficiency
  • Management: Tx the underlying cause, bicarb controversial, studies have shown no benefits? But most experts would agree with usage in critically ill patients with profound acidemia.

 

MALA: Lastly, this case illustrates the dangers of metformin, in the right setting, can lead to severe acid/base disturbance (MALA).

  • Do NOT use metformin if GFR < 30, be careful in CKD patients.
  • If suspecting metformin toxicity and pt is hyperglycemic, this is a sign of severe toxicity.
  • Always do a thorough med reconciliation on every single patient!