AM Report 4/10/17 Gastric Bezoar

Definition: a foreign body resulting from accumulation of ingested material – most commonly found as a hard mass / concentration in the stomach.

Types

Phytobezoar: composed of vegetable matter – MOST COMMON

phytobezoar

Trichobezoar: composed of hair

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Pharmacobezoar: composed of ingested medications

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Other: composed of a variety of other substances (tissue paper, shallac, fungus, styrofoam, cement, etc.)

Pathogenesis

  • Ingestion of indigestible material
  • Delayed gastric emptying
  • Composition / Interaction with gastric material – unripe persimmon fruit contain shibuol (soluble tamin), which forms coagulate when mixed with gastric material

Rapunzel Syndrome: trichobezoar from the stomach to the terminal ileum

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Epidemiology: RARE

  • Incidence ~0.3% on EGD
  • Phytobezoars – male ~40-50 years old
  • Trichobezoars – female ~20s; associated with underlying psychiatric disorder

Risk Factors:

  • Gastric dysmotility – underlying anatomic abnormality may predispose to formation
    • 70-94% have had gastric surgery
    • 54-80% have undergone vagotomy / pyloroplasty
  • Gastroparesis
  • Gastric outlet obstruction
  • Dehydration
  • Medications – insoluble carrying vehicle, high hygroscopy

Clinical Manifestations:

  • Abdominal pain
  • Nausea/vomiting
  • Early satiety
  • Anorexia
  • Weight loss
  • GIB/Obstruction – NOT COMMON

Physical exam: unremarkable in most, occasional abdominal pain and halitosis.  Alopecia in trichobezoars.

Imaging:

  • Abdominal radiograph with/without barium
  • Abdominal US
  • CT scan

Complications:

  • GI perforation
  • Peritonitis
  • Protein-losing enteropathy
  • Steatorrhea
  • Pancreatitits
  • Intussusception

Diagnosis:

  • EGD is required to establish the diagnosis of a gastric bezoar AND to obtain samples to determine composition/type

Management: controversial in the absence of studies comparing different modalities

  • Chemical dissolution – administration of an agent to degrade the gastric bezoar (non-invasive / inexpensive); potential complication of SO from partially dissolved bezoars ~ 6 weeks later
    • Coca-cola – 3L/12H; low pH, mucolytic effect, ↑ sodium bicarb content, CO2 bubbles (widely available, inexpensive, well-tolerated)
    • Cellulase – dissolves cellulose found in plant fiber / phytobezoars
    • Papain – type of meat tenderizer with many complications
    • Acetylcysteine – low success rates (~50%)
  • Endoscopic removal – fragmenting the bezoar with water jet, direct suction (large channel), forceps, snares; allow the fragments to be cleared.
  • Adjuvant prokineticsMetoclopramide typically used in conjunction with endoscopic / chemical therapy because it may decrease the time to dissolution.
  • Surgery – reserved for patients that fail chemical AND endoscopic treatment OR those with complications (obstruction/bleeding) OR when composition is not amendable to either other treatment options.

AM Report 4/6/17: Epiglottitis

Wheezes: “All that wheezes is not asthma, but all that wheezes is obstruction.”

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Extrathoracic Upper Airway

Nasopharynx & Oropharynx

  • Tonsillar Hypertrophy
  • Pharyngitis
  • Peritonsillar abscess
  • Retropharyngeal abscess

Larynogpharynx & Larynx

  • Epiglottis
  • Paradoxical Vocal Cord Movement
  • Vocal Cord Paralysis
  • Anaphylaxis & Laryngeal Edema
  • Post Nasal Drip
  • Benign/Malignant Tumors
  • Relapsing Polychondritis (subglottic stenosis)

Intrathoracic Upper/Lower Airways

Trachea

  • Tracheal stenosis
  • Tracheomalacia
  • Goiter

Proximal Airways

  • Foreign-body aspiration
  • Bronchitis

Distal Airways

  • Asthma
  • COPD
  • Pulmonary edema
  • Bronchiectasis

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“Thumb sign” of epiglottitis

Infectious causes of epiglottitits

Bacterial:

  • H. influenza (type B)
  • Steptococcus pneumoniae
  • Staphylococcus aureus (MRSA/MSSA)
  • B-hemolytic streptoccoci (A-G)

Viral:

  • HSV
  • VZV
  • EBV
  • Para/Influenza

Non-Infectious

  • Thermal injury
  • Foreign body

Risk Factors:

Children: incomplete/lack of immunizations; immune deficiency

Adults: comorbid condition (HTN, DM, PSA, etc.), immune deficiency

3 D’s of Epiglottitis – Drooling, Dysphagia, Distress

Presentation:

Children: respiratory distress, anxiety, posture (see below), stridor, muffled (hot potato) voice.

Tripod Posture / Sniffling Position:

Adults: sore throat/odynophagia (~90%), fever, muffled voice, drooling, stridor/respiratory distress, hoarseness

Onset:

Children: <24 hours (frequently <12 hours)

Adults: 48 hours (65%)

Treatment:

First – secure airway!

Next – empiric antibiotics (typically 3rd generation cephalosporin and MRSA coverage)

 

AM Report 3/27/17: Weakness

Myasthenia Gravis: autoimmune – directed against post-synaptic NM junction; look for bulbar muscle involvement that gets worse with activity.

Sign/Symptoms:

  1. Ocular: ptosis/diplopia, EOM involvement, no pupillary involvement
  2. Bulbar: dysarthria, dysphagia, fatigue with chewing
  3. Weakness: proximal limb weakness, facial/neck weakness
  4. Respiratory muscle weakness ⇒ Myasthenia crisis

Tests:

Bedside

  • Ice-pack test – improved ptosis with ice pack administration
  • Tensilon (edraphnium) – acetylchoinesterase inhibitor with rapid onset/short duration; NOT SPECIFIC

Serologic

  • Acetylecholine receptor antibody
  • Muscle specific tyrosine kinase antibody (Anti-MUSK)

Electrophysiologic

  • Repetitive nerve stimulation: ↓ amplitude with repetitive stimulation ~75% have thymic abnormalities (85% thymic hyperplasia, 15% thymoma)

GBS: ascending motor and sensory involvement, symmetric

Timing: <4 weeks

Pathophysiology: Due to molecular mimicry → immune response to preceding infection cross reacts to peripheral nerve

Common trigger: Campylobacter Jejuni (most common), CMV, EBV, HIV, VZV, mycoplasma, Zika

Physical Exam:

  • Absent/depressed DTRs (90%)
  • Ascending weakness (~90%)
  • Paresthesias (80%)
  • Facial weakness/bulbar signs (55%)

LP: Albumino-cytologic dissociation

Miller Fisher Variant

  • Ophthalmoplegia
  • Ataxia
  • Areflexia

Botulism: bulbar involvement – spread in craniocaudal direction ~ “descending paralysis” with CN/eye involvement

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AM Report 3/22/17: Pleural Effusion

Most common etiologies for BLOODY pleural effision:

  • Trauma
  • Malignancy
  • Pulmonary infarct
  • Post-cardiac injury

Lights Criteria: one criteria = EXUDATIVE effusion

  1. Pleural total protein / serum total protein > 0.5
  2. Pleural LDH / serum LDH > 0.6
  3. Pleural LDH ≥ 2/3 ULN for serum LDH

* Lights criteria is SENSITIVE, but NOT SPECIFIC – you do not want to miss an exudative effusion, so you want to a low false negative rate.

* For patients with a high suspicion for transudative effusion, but meets Lights criteria (i.e. CHF following initiation of diuresis), check serum albumin and pleural albumin (if serum – pleural < 1.2 mg/dL, confirms diagnosis of exudative effusion).

Transudative Effusions (not a complete list):

  • CHF (~90%)
  • Cirrhosis (hepatic hydrothorax)
  • Severe hypoalbuminemia
  • Nephrotic syndrome
  • Peritoneal dialysis
  • Myexedma
  • Constrictive pericarditits
  • SVC syndrome

Exudative Effusion (not a complete list):

  • Infection (PNA/TB)
  • Malignancy
  • CTD
  • Pancreatitis
  • Trauma
  • PE/Pulmonary infarct
  • Post heart surgery
  • Esophageal rupture

If exudative effusion, start with cell count/diff

  • PMNs > 50% – parapneumonic, PE, pancreatitis
  • Lymphs > 50% – Cancer, TB, fungal, post-surgery
  • Eosinophils >10% – Hemothorax, drug reaction, parasite infection

AM Report 04/11/17 Hypothyroid Myopathy

Myopathy is not only due to trauma, crush injury or statins! 

Etiologies of non-traumatic-non-exertional rhabdomyolysis (elevated CK)

ALCOHOL, illicit drugs- from A (methAmphetamine) to Z (ecstasy), all are associated with rhabdo
Medical drugs, commonly statins/fibrates but MANY implicated drugs (see below
-Infectious (including HIV!)
-Seizures, DTs, or restraints (avoid prolonged restraints of this reason and re-assess need for them frequently
Hypothyroidism (more on this later)-Check that TSH!
-NMS, Malignant Hyperthermia
Inflammatory myopathies(Dermatomyositis/Polymyositis/Dermatomyositis)
Electrolyte abnormalities (eg: HypoK, HypoPhos)

List of implicated drugs (not a comprehensive list)


Make sure you do a comprehensive history when evaluating for rhabdo and consider secondary causes per above, including meds and thyroid abnormalities

What are some manifestations of SEVERE hypothyroidism (Myxedema Coma)

-See our other blog post for more details but the THREE cardinal features of Myxedema Coma are ALTERED MENTAL STATUS (not commonly Coma as the name states), HYPOthermia, and a PRECIPITATING EVENT (commonly an infection, or cold exposure, or MI or trauma)
-The “classic” patient who gets Myxedema Coma is an elderly female >60 years with history of untreated hypothyroidism presenting during the winter months. However, classic is not always so classic.
-Other findings include Bradycardia, HYPOnatremia, HYPOglycemia, and HYPOtension

Treatment of Myxedema Coma

IV Levothyroxine (L4, sometimes L3 but controversial) along with stress dose steroids unless adrenal insufficiency is ruled out (get that AM cortisol!). Otherwise you can precipitate an ADRENAL CRISIS

What does hypothyroid myopathy look like? 

-Elevation in CK usually less than 10x ULN (seen in 60-90 % of patients), usually triggered by intense exercise or concurrent statin therapy (like our patient)
Muscle hypertrophy (thickened doughy appearance of skin and subQ tissues)
Proximal myopathy (progressive symmetric proximal weakness- can look like an inflammatory myopathy!)

Treatment

-Treat the hypothyroidism and symptoms usually improve

Take home point

-Did I mention that hypothyroidism is a common etiology of rhabdomyolysis?

AM report 03/23/17 Monoclonal Gammopathies: Waldenströms

What is a monoclonal gammopathy?

-Proliferation of single clone of plasma cells (M protein)
-Remember M is for monoclonal, not for IgM
-Can be detected in serum and/or urine
-M protein consists of heavy chain complexed with kappa/lambda light chain or free kappa/lambda light chain. See our patient’s spike below!

monoclonal gammopathy

What can cause a monoclonal gammopathy?

-Although we commonly think about malignant processes, there are BENIGN etiologies including CTD, vasculitis, viral infections, or even post-transplant. See below for example from BCMJ

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Credit: http://www.bcmj.org/articles/monoclonal-gammopathy-and-primary-care

What tests should you order next if you suspect a monoclonal gammopathy?

-Start with LFTS and look at your TOTAL PROTEIN and ALBUMIN level. If you see a high TP and a low albumin (high protein gap), you should worry that there is a monoclonal gammopathy
SPEP and UPEP and allow measurement of the concentration of the M protein but does NOT tell you the isotype. For that you need to do the next step
-Confirm with IMMUNOFIXATION and check free light chain assay (FLC)
-Serum Immunoglobulins can tell if you high or low but do not establish the clonality 

What are the diagnostic criteria for Waldenstrom’s Macroglobulinemia?

IgM (remember to flip that W to remember that Waldenstroms has an IgM spike) monoclonal gammopathy of any size
Greater than 10 % of Bone Marrow Biopsy show lymphoplasmacytic features
-Typical immunophenotype (B cell markers eg: CD20)

Clinical Manifestations

-Can be ASYMPTOMATIC! known as Smoldering Waldenstroms
-Due to IgM deposition, can see peripheral neuropathy and hyperviscosity syndrome.

Hyperviscosity Syndrome is a LIFE-THREATENING EMERGENCY that is treated with Plasma Exchange and symptoms can be non-specific (blurry vision, epistaxis, headache, vertigo but can cause stroke, coma or even CHF)
-Diagnosis of Hyperviscosity syndrome is CLINICAL but unlikely unless Serum Viscosity >4 CP (Centipoises) and IgM spike>4. Remember that Plasma Exchange does NOT treat the underlying cause!

-Due to infiltration, can see anemia, hepatosplenomegaly, and lymphadenopathy
-Bleeding manifestations, most commonly EPISTAXIS, but can be non-specific like fatigue, weakness, and weight loss

What are two associations with Waldenstrom’s to keep in mind?

-Associated with Type I Cryoglobulinemia (SMV with palpable purpura)
Cold agglutinin hemolytic anemia (AIHA with +DAT)

Treatment of Waldenstroms

-If asymptomatic, does NOT need to be treated but risk of developing symptoms
-If hyperviscosity syndrome==>Plasma Exchange
Medical therapy includes TKI (eg: Ibrutinib), alkylating agents (eg: Bendamustine), purine analogs (eg: Cladribine), steroids and HSCT if candidate.
-AVOID PRBC transfusions if possible as can worsen hyperviscosity. 

AM Report 03/09/17: Palpable Purpura (Small Vessel Vasculitis)

Is it Purpura, Petechiae or Ecchymoses?

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Common etiologies of Palpable Purpura (histologically identified as leukocytoclastic vasculitis) 

-Infections (eg: HIV, HBV, HCV, endocarditis among other viral infections)
MEDICATIONS (many medications most commonly NSAIDS, cephalosporins, NSAIDS)
-Malignancies (eg: Paraneoplastic syndrome)
Vasculitis (small vessel vasculitis)-see below.

When you think of palpable purpura with systemic symptoms, think about small vessel vasculitis. If NO systemic symptoms, think about cutaneous small vessel vasculitis (CSVV)

Types of Small vessel vasculitis (SVV)

-Cryoglobulinemic vasculitis
-IgA vasculitis (HSP)
-ANCA associated Small Vessel Vasculitis (MPA, GPA, EGPA)
-NON-ANCA mediated (Infections, drug induced, CTD, Sjogrens, Goodpastures etc.)

vasculitis.png

How do you workup new onset vasculitis with palpable purpura?

-CBC, Chem 7, LFT, ESR, CRP
-Viral hepatitis panel + HIV
-Serum cryoglobulins
-Urinalysis for proteinuria or GA
-Blood cultures (rule out endocarditis)
-ANA (auto-immune)
-C3,C4 (low levels in cryoglobulinemia, SLE)
-ANCA
-CXR , CT (evaluate hemoptysis with DAH)
-Often skin biopsy is not necessary but can support diagnosis.

Treatment

-Treat the underlying etiology, often requiring immunosuppression