Hyperemesis Flashcards

1
Q

Definition of hyperemesis gravidarum

A

Nausea and/or vomiting caused by pregnancy leading to significant reduction of oral intake
and weight loss of at least 5% compared with pre-pregnancy, with or without dehydration and/or
electrolyte abnormalities.

SOMANZ definition

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2
Q

Evaluate 2 scoring systems for assessing the severity of HG

A

Rhodes score

PUQE- Pregnancy-Unique
Quantification of Emesis and Nausea
PUQE more simple than Rhodes score

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3
Q

Incidence of HG?

Natural history of HG?

A

1%

50% of women start to have resolution of sx by week 14, majority by week 22

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4
Q

Risk factors for HG

A
- High HCG e.g. due to trophoblastic disease, twins 
Mixed evidence for: 
- Pre-existing H Pylori 
- deficiency of trace elements, 
- excess thyroid hormones, 
-Gravidity, 
- fetal female sex, 
- psychiatric
- dietary factors
- Family history
- black or asian ethnicity
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5
Q

Hx and examination of women with HG

A

History and physical examination should be directed towards identification of alternate diagnoses.
Physical examination should include assessment of temperature, weight, palpation of the abdomen for
abdominal tenderness and signs of peritonism, and an assessment for neck stiffness and signs of
raised intracranial pressure if the history is suggestive of a central nervous system cause for the
symptoms.

Signs to support a diagnosis of dehydration include decreased skin turgor, dry mucous
membranes, decreased urine output, concentrated urine, and postural drop in blood pressure

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6
Q

Investigations for HG

A
  1. Sodium, potassium, chloride, bicarbonate, magnesium, urea and creatinine
  2. Bilirubin, Alanine Transaminase (ALT), Aspartate Aminotransferase (AST), Albumin
  3. Obstetric ultrasound to exclude multi-fetal or gestational trophoblastic disease
  4. Tests to exclude alternate diagnoses where indicated
  5. Thyroid stimulating hormone (TSH) where indicated, TFTs frequently abnormal but usually normalise and rarely require treatment
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7
Q

Management

A
  • Try to provide ambulatory care where possible
  • Rehydration
  • If severe HG and admitted for IVF then repeat U+Es
  • Metaclopramide and Ondansetron should be second line antiemetics due to metaclopramides risk of extrapyramidal side effects and Ondansetrons minimal safety data
  • Replace thiamine either PO or IV
  • Consider clexane for women admitted to hospital
  • Steroids when standard therapies have failed
  • If severe- consider MDT, with dieticians, therapists, psych if needed etc
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8
Q

Complementary therapies for HG

A

Ginger- several systematic reviews have found evidence that ginger improves the symptoms of N+V when compared to placebo

Acustimulations – acupressure and acupuncture. Some improvement in systematic review to support the use of accupressure. No evidence of harm in pregnancy.

Hypnosis- no evidence

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9
Q

When should inpatient management of HG be considered?

A
  • continued N&V with inability to keep down antiemetics
  • continued N&V with >5% weight loss and/or ketonuria
  • confirmed/suspected comorbidity (eg UTI and unable to keep down PO ABx)
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10
Q

Why is dextrose fluid not recommended for fluid replacement in HG?

A
  1. Risk of precipitating Wernickes encephalopathy in thiamine deficiency
  2. Risk of central pontine myeolinolysis in hyponatraemia
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11
Q

Proposed theories of HG?

A
  • Caused by rise in HCG
  • Relaxation of oesophageal sphincter and decreased gastric motility
  • May be linked to thyroid hormones as many women found to have raised thyroid hormones in HG
  • Possibly due to nutrient deficiency
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12
Q

Investigations for HG?

A

Urine dipstick:
– quantify ketonuria as 1+ ketones or more
G MSU
G Urea and electrolytes:
– hypokalaemia/hyperkalaemia
– hyponatraemia
– dehydration
– renal disease
G Full blood count:
– infection
– anaemia
– haematocrit
G Blood glucose monitoring:
– exclude diabetic ketoacidosis if diabetic G Ultrasound scan:
– confirm viable intrauterine pregnancy
– exclude multiple pregnancy and trophoblastic disease
G In refractory cases or history of previous admissions, check:
– TFTs: hypothyroid/hyperthyroid
– LFTs: exclude other liver disease such as hepatitis or gallstones, monitor malnutrition
– calcium and phosphate
– amylase: exclude pancreatitis
– ABG: exclude metabolic disturbances to monitor severity

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13
Q

Differential diagnosis of HG

A
peptic ulcers, 
cholecystitis, 
gastroenteritis, 
hepatitis, 
pancreatitis, 
genitourinary conditions such as urinary tract infection or pyelonephritis, 
metabolic conditions, 
neurological conditions
drug-induced nausea and vomiting.
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14
Q

When should inpatient management be considered?

A

Continued nausea and vomiting and inability to keep down oral antiemetics

ketonuria and/or weight loss (greater than 5% of body weight), despite oral antiemetics

Confirmed or suspected comorbidity (such as urinary tract infection and inability to tolerate
oral antibiotics).

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15
Q

Advice for future pregnancies?

A

HG likely to recur

Some evidence to support pre-emptive antiemetics, found to reduce severity of HG in subsequent pregnancy

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16
Q

Ginger

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A

MOA: Improvement in gastrointestinal motility: weak effect on cholinergic M3 receptors and serotonergic 5-HT3 and 5-HT4 receptors in the gut

Efficacy: reduces N but not V
Superior to placebo
Equal to Vitamin B6, dimenhydrinate, metoclopramide, doxylamine, P6 (LOE- II)

Dosing: up to 1200 mg/day split doses eg 250 mg QID

SE: Drowsy, heartburn

Teratogenesis: NA

Practice points:
Theoretical risk of bleeding risk by decreasing platelet-aggregation.
May inhibit growth of Helicobacter Pylori

17
Q

Vitamin B6

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A

MOA
Water soluble vitamin, inhibits H1 receptor, acts indirectly on vestibular system, some inhibition of muscarinic receptors to decrease stimulation of vomiting centre

Efficacy
Reduces N but not V

Dosing
10 to 25 mg PO 3-4x/day Up to 200 mg/day
Or 37.5 mg combined with ginger 600 mg up to 2x/day

SE
Sensory neuropathy

Teratogenesis - NA

Practice points
More effective when used in combination eg with doxylamine or dicyclomine (equivalent to metoclopramide)

18
Q

Histamine antagonist - Cyclizine

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A

MOA
Indirectly affect the vestibular system, decreasing stimulation of the vomiting centre

Efficacy
Minimal evidence to support

Dosing
50mg TDS

SE
Sedation, anticholinergic effects

Teratogenesis
NA
Practice points

19
Q

Dopamine antagonist: Metaclopramide

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A

MOA
Dopamine and serotonin receptor antagonist which stimulates upper gastrointestinal motility and acts on CNS vomiting centre

Efficacy
Equal to ondansetron for N but less effective for V

Dosing
10mg TDS

SE
Less sedation, akathisia, depression.
Rare: tardive dyskinesia with chronic use
IV: occulogyric crisis

Teratogenesis: nil

Practice points:

20
Q

Phenothiazines: e.g. prochlorperazine

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A

MOA
Central and peripheral dopamine antagonists

Efficacy: superior to placebo

Dosing: 5-10mg TDS

SE: Sedation, akathisia, anticholinergic effects, hypotension Rare: dystonias, tardive dyskinesia with chronic use

Teratogenesis: nil

21
Q

Ondansetron

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A

Mechanism of action
Central (medullary vomiting centre) and peripheral (small bowel) serotonin receptor blocker

  • Efficacy: superior compared to several others
  • Recommended/max dose: 4-8mg TDS
  • Side effects
    Constipation, headache, dizziness
  • Risk of teratogenesis
    Conflicting data but does not appear to increase overall risk of birth defects
  • Practice points
    No sedation
    Expensive
    Available as tablets, wafers and oral dispersible formulations Ensure concurrent management of constipation-bowel obstruction has been reported Recommended as second line agents
22
Q

Steroids

  • Mechanism of action
  • Evidence for efficacy
  • Recommended/max dose
  • Side effects
  • Risk of teratogenesis
  • Practice points
A
  • Mechanism of action
    Antiemetic effect on the chemoreceptor trigger zone in the brainstem
  • Evidence for efficacy
    Improved sense of wellbeing, appetite and increased weight gain in HG patients No difference in days of hospital admission or readmission rates compared to placebo
  • Recommended/max dose
    Prednisone 40-50 mg/day. (May be commenced as hydrocortisone 100 mg IV BD)
  • Side effects
    Potential Cushing’s syndrome, mood disturbance, hypertension, hyperglycemia
  • Risk of teratogenesis
    Possible increased risk of oral clefts when used < 10 week’s gestation, but data are weak
  • Practice points
    Consider withholding until after 10 weeks gestation if alternate therapy an option
    Restrict to refractory cases
23
Q

Severe sequelae of HG

A

Wernicke’s encephalopathy (vitamin B1 deficiency),
bleeding diathesis (vitamin K deficiency),
acute kidney injury,
splenic avulsion,
oesophageal rupture,
pneumo-mediastinum and rhabdomyolysis