Rosen & Barkin's 5-Minute Emergency Medicine Consult (362 page)

• IV, monitor if signs of significant volume depletion
  
• IV hydration
  

IV hydration using a crystalloid solution (LR or NS)

• IV hydration using LR or NS
  
• Dextrose may be added to help break cycle of ketosis
  
• Treat until patient is no longer symptomatic from hypovolemia
  
• Antiemetics administered IV are given to break the vomiting cycle
  
• Most commonly used medications:
  
  • Metoclopramide:
    
    • FDA category B
      
  • Promethazine and prochlorperazine:
    
    • Both FDA category C
      
    • Recent FDA warning regarding complications of IV promethazine administration
      
  • Ondansetron:
    
    • FDA category B with recent warning about the risk of prolonged QT syndrome and the recommendation for ECG monitoring of the patient with electrolyte abnormalities such as hypokalemia or hypomagesemia
      
  • These have been used extensively in pregnancy, and there is little or no evidence associated with increased risk of congenital anomalies
    
  • Antiemetics are preferable to the risk of prolonged ketosis and hypovolemia
    
• Oral rehydration in the ED after the initial fluid resuscitation and antiemetics
  
• Thiamine 100 mg IV/IM/PO in the patient who requires IV rehydration due to case reports of Wernicke encephalopathy
  
• Antihistamines have been shown to be effective
  
• Methylprednisolone may be effective for patients with hyperemesis gravidarum:
  
  • Last resort
    
  • Avoid if <10 wks gestation
    

• Metoclopramide (category B): 10–20 mg IV
  
• Ondansetron (category B): 4–8 mg IV or 4 mg PO or ODT every 8 hr
  
• Prochlorperazine (category C): 5–10 mg IV not to exceed 40 mg/d
  
• Promethazine (category C): 12.5–25 mg IM
  
• Discharge outpatient medications:
  
  • Meclizine (category B): 25 mg PO q6h PRN
    
  • Metoclopramide (category B): 10 mg PO q6–8h PRN
    
  • Prochlorperazine (category C): 5–10 mg PO q6h or 25 mg PR q12h PRN
    
  • Promethazine (category C): 12.5–25 mg PO or PR q4–6h PRN
    
  • Pyridoxine (vitamin B
    ₆
    ; category A): 25 mg PO TID (OTC)
    
  • Ginger (
    Zingiber officinale
    ): 500–1500 mg div. bid/tid
    
  • Doxylamine (Unisom—OTC) 12.5 mg PO q6–8h usually with pyridoxine (vitamin B
    ₆
    )
    
  • Thiamine: 50 mg PO per day for symptoms >3 wks
    

Methylprednisolone (category C): 16 mg IV or PO q8h × 3 days and then taper. Should be prescribed in consultation with obstetrician.

FOLLOW-UP

• Inability to tolerate oral intake after treatment
  
• Inability to control the emesis despite treatment
  
• Severe electrolyte or metabolic disturbances
  
• At highest risk <8 wk gestation
  

• Most patients can be discharged as long as they are able to tolerate oral intake and have adequate follow-up
  
• Correction of dehydration and associated symptoms
  
• Decreased ketonuria
  
• Reassure patient that their symptoms are common and usually self-limited
  
• Patients should be counseled that frequent, small meals may be helpful:
  
  • Meals should contain simple carbohydrates and be low in fats
    
  • Avoid irritant or spicy foods
    
• Home IV therapy can be arranged if indicated
  

• All patients with diagnosis should take at least 3 mg thiamine/day to help prevent Wernicke encephalopathy; a supplement of 50 mg/day PO is recommended
  
• Risk for 1st trimester fetal loss is less in women with hyperemesis
  

• Other diagnoses should be explored in patients presenting after 9 wk gestation with nausea and vomiting as initial symptoms
  
• The use of PICC lines has been shown to carry significantly increased risk of maternal morbidity when compared to patients managed with either NG tube or medications alone
  
• Be aware of the risk for central pontine myelinosis in hyponatremia patients when replacing sodium
  
• Wernicke encephalopathy is the most devastating maternal complication:
  
  • Patients may not have the classic triad of ataxia, nystagmus, and dementia. Be concerned for any evidence of apathy or confusion
    
  • Be sure to give patients thiamine 100 mg IV for any patient who presents with apathy or confusion
    

• Bottomley C, Bourne T. Management strategies in hyperemesis.
  Best Prac Res Clin Obstet Gynaecol
  . 2009;23:549–564.
  
• Goodwin TM. Hyperemesis gravidarum.
  Obstet Gynecol Clin North Am
  . 2008;35(3):401–417.
  

CODES

• 643.00 Mild hyperemesis gravidarum, unspecified as to episode of care or not applicable
  
• 643.10 Hyperemesis gravidarum with metabolic disturbance, unspecified as to episode of care or not applicable
  

BASICS

• Potassium distribution:
  
  • Extracellular space: 2%
    
  • Intracellular space: 98%
    
• Potassium excretion:
  
  • Renal: 90%
    
  • GI: 10%
    
• Renal (80–90%) and extrarenal mechanisms maintain normal plasma concentration between 3.5 and 5 mmol/L.
  
• Renal excretion of potassium affected by:
  
  • Dietary intake
    
  • Distal renal tubular function
    
  • Acid–base balance
    
  • Mineralocorticoids
    
• Regulation between intracellular and extracellular potassium balance is affected by:
  
  • Acid–base balance
    
  • Insulin
    
  • Mineralocorticoids
    
  • Catecholamines
    
  • Osmolarity
    
  • Drugs
    

• Decreased potassium excretion:
  
  • Most common cause: Renal failure (acute or chronic)
    
  • Distal tubular diseases:
    
    • Acute interstitial nephritis
      
    • Renal transplant rejection
      
    • Sickle cell nephropathy
      
    • Renal tubular acidosis (diabetes)
      
  • Mineralocorticoid deficiency:
    
    • Addison disease
      
    • Hypoaldosteronism
      
  • Drugs:
    
    • ACE inhibitors/angiotensin receptor blockers
      
    • β-blockers
      
    • Potassium-sparing diuretics
      
    • NSAIDs
      
    • Cyclosporine
      
    • High-dose trimethoprim
      
    • Lithium toxicity
      
• Intracellular to extracellular potassium shifts:
  
  • Metabolic acidosis:
    
    • Serum K
      ⁺
      rises 0.2–1.7 mmol/L for each 0.1 U fall in arterial pH.
      
  • Hyperosmolar states
    
  • Insulin deficiency
    
  • Cell necrosis
    
  • Rhabdomyolysis
    
  • Hemolysis
    
  • Chemotherapy
    
  • Drugs:
    
    • Digitalis toxicity
      
    • Depolarizing muscle relaxants (e.g., succinylcholine)
      
    • β-blockers
      
    • α-agonists
      
  • Hyperkalemic periodic paralysis
    
• Excess exogenous potassium load:
  
  • Cellular breakdown:
    
    • Trauma
      
    • Tumor lysis
      
  • Salt substitutes
    
  • Oral potassium
    
  • Potassium penicillin G
    
  • Rapid transfusions of banked blood
    
• Pseudohyperkalemia:
  
  • Traumatic venipuncture with hemolysis
    
  • Postvenipuncture release of potassium can occur in the setting of:
    
    • Thrombocytosis (platelets >800,000/mm
      ³
      )
      
    • Extreme leukocytosis (WBC >100,000/mm
      ³
      )
      
  • Prolonged tourniquet time
    

DIAGNOSIS

• Hyperkalemia is often asymptomatic, even at high levels.
  
• Neuromuscular symptoms, predominantly weakness, which can progress to paralysis.
  
• Dyspnea owing to respiratory muscle weakness.
  
• Cardiac dysrhythmias may be the initial manifestation, so patients could also present with chest pain, palpitations, or syncope.
  

• Muscular weakness (rare except in severe cases)
  
  • Paralysis has been described
    
• Cardiac dysrhythmias (see ECG Changes)