Variceal Bleeding

Active Gastroesophageal Varices bleeding

 

Background: 

Gastroesophageal varices bleeding is associated with a mortality rate approaching 20-30%.  

Bleeding from varices stops spontaneously only in 50% of patients



Evaluation: 

History: 

Prior complications, medications, fever, abdominal/chest pain, vomiting, melena, syncope/pre-syncope, hematemesis, cause of cirrhosis, prior interventions on varices, weights.

Exam: 

Evaluate hemodynamic status immediately (consider use of beta blockers). 

Look for signs of chronic liver disease – spider angiomata, palmar erythema, jaundice, ascites (shifting dullness, fluid wave, etc.), coagulopathy (petechiae, purpura), ENT exam (pharynx), CV, pulmonary, extremities, mental status.

Labs

ECG, CBC, coags, renal function, VBG/lactate, Ammonia level, electrolytes, LFTs, type and cross, fibrinogen, CXR and EKG 




Management: 

First obtain bilateral IV access (large bore advised), monitors, supplemental oxygen. Wear personal protective equipment. 

 

Airway: 

This is one of the most difficult airways to management due to shock state, difficulty with visualization, rapid desaturation with sedative/paralytic, and extensive blood loss.

Use NG tube to decompress stomach (remove the ticking time bomb). 

May use metoclopramide 10 mg or erythromycin 250 mg IV to assist in moving blood through GI tract

Place in Trendelenberg if vomiting (keep blood out of lungs).




Bleeding and Circulation:

Hemostatic Resuscitation: Do not rely on PT/PTT/INR to assess coagulation status. Consider use of TEG instead. May need to start MTP

Consider pRBCs if Hb <7 g/dL (goal of Hb between ≥7 g/dL (70 g/L) and <9 g/dL). If pt received >6 units of pRBCs in <3 hours check serum ionized calcium concentration (due to citrate binding of ionized calcium) 

Platelets – if initial platelet count is < 50,000/microL 

Prohemostatic products – consider fresh frozen plasma, PCC on case by case basis, cryoprecipitate targeting fibrinogen 150-200 mg/dL. Consider to use TXA 1g IV. 



Target resuscitation end points of mentation, capillary refill, MAP, urine output. 




Source Control: Emergency GI and IR consults. 

May use erythromycin or metoclopramide to improve view for EGD. 

Use octreotide 50 mcg IV bolus, 50 mcg/hr IV infusion (or vasopressin with nitroglycerin), which is associated with decreased products transfused. 



Be ready with other devices: Sengstaken-Blakemore, Minnesota, Linton-Nachlas tubes.

https://www.youtube.com/watch?v=Yv4muh0hX7Y



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Prevent and Treat Complications

Infection associated with 25-65% of upper GI bleeds from varices (UTI, SBP, pneumonia):

Ceftriaxone 1 g IV or cefotaxime 2 g IV associated with NNT of 22 to prevent death and NNT of 4 to prevent infection. 

Albumin also useful in patients meeting certain criteria (Cr 1.5, BUN > 30, bilirubin > 4)

Consider NG tube placement for stomach decompression (Whether placement of a nasogastric tube can help prevent aspiration has not been well studied)

Beware of renal failure and encephalopathy, which are further complications.

 

References: EMCrit, EMDoc, UpToDate








ECG: What about U waves?

ECG 1.png

 

What is the U wave? 

Small 0.5mm deflection following T wave: and best seen in V2 and V3 

Usually in the same direction as T wave 

Usually better visible at slow heart rates < 65 bpm

Grows bigger as HR decreases

Usually < ¼ of the T wave voltage, if much bigger (or >2mm)- its abnormal

 

Where is it coming from?

May be Purkinje fibers repolarization

May be some kind of after-potential

No one really knows

 

Abnormal U waves:

Prominent U wave - >1-2mm or 25% of the height of the T wave

Common causes: 

Bradycardia

Severe hypokalemia.

Hypocalcaemia

Hypomagnesaemia

Hypothermia

Raised intracranial pressure

Left ventricular hypertrophy

Hypertrophic cardiomyopathy

 

Drugs associated with prominent U waves:

Digoxin

Phenothiazines (thioridazine)

Class Ia antiarrhythmics (quinidine, procainamide)

Class III antiarrhythmics (sotalol, amiodarone)

 

Hypokalemia

EKG3.png

 

U waves associated with left ventricular hypertrophy

EKG4.jpg


U waves associated with digoxin use

 Inverted U waves:

A negative U wave is highly specific for the presence of heart disease

Common causes of inverted U waves

Early MI

Coronary artery disease

Hypertension

Valvular heart disease

Congenital heart disease

Cardiomyopathy

Hyperthyroidism

 

Inverted U waves in a patient with NSTEMI 

EKG6.jpg


References: UpToDate. LITFL, ecg.utah.edu, ecg weekly

 

 

 







 · 

Thyroid storm



Thyroid Storm

 

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Background

 

Thyroid storm is a rare yet mortality rates reported between 10-30%

It is often presents in patients (pts) with established hyperthyroid disease (Graves' disease, toxic multinodular goiter, solitary toxic adenoma)

 

Precipitating Factors: Trauma, infection, DKA, CVA, PE, MI, etc.

 

Presentation and Diagnosis

 

Thyroid storm is a clinical diagnosis of a severe and exaggerated form of thyrotoxicosis.  

Look for a triad:

Extreme Fever (often >104F)

Tachycardia (can be accompanied with AFib, widened pulse pressure)

Altered Mental Status



Other findings:

Tremor

Lid Lag

Proptosis/Periorbital Edema

Pretibial plaques/nodules/non-pitting edema

Goiter/Thyroid Nodules

 

 

Labs:

low TSH and high free T4 and/or T3 concentrations

mild hyperglycemia, mild hypercalcemia, abnormal liver function tests, leukocytosis, or leukopenia

 

 

Management

 

Supportive Care

Fever: Cooling measures and antipyretics. 

Agitation: Benzodiazepines 

Vascular instability: IV fluids

 

Beta Blockers:

β blockade is critical in the management of the peripheral actions of increased thyroid hormone.

Propranolol 0.5-1mg IV over 10 mins followed by redosing 1-3mg every few hours OR 60-80mg PO q4h

Alternative metoprolol, esmolol or atenolol 



Thionamides - Inhibit New Synthesis by blocking T4-to-T3 conversion

PTU for the acute treatment of life-threatening thyroid storm -

Propylthiouracil (PTU) 600-1000mg PO loading dose with 200-400mg PO q6-8h, Hepatotoxic

Methimazole for severe, but not life-threatening for a longer duration of action 

Methimazole 20-25mg PO q4-6h - longer half-life compared to PTU.



Iodines - blocks the release of pre-stored hormone, and decreases follicular transport and oxidation.

SSKI 5 drops PO q6h or Lugol’s Solution 4-8 drops PO q6-8h

Works through “Wolff-Chaikoff effect,” in which high levels of iodide will inhibit T3/T4 synthesis and release

Give AFTER antithyroid drugs, no sooner than 30-60 mins following PTU/Methimazole.

Lithium 300mg PO q6-8h - for iodine allergy or contraindication to iodine usage 

 

Other therapies to consider: 

Steroids (Inhibit Peripheral Conversion) Hydrocortisone 300mg IVx1 and then 100mg IV q8h or Dexamethasone 2-4mg IV q6h

Cholestyramine (4 g orally four times daily) - bile acid sequestrants to reduce enterohepatic circulation of thyroid hormone

Plasmapheresis: Offers temporary stabilization for a patient that has been unresponsive to antithyroid medications



References: EMDocs, UpToDate