Vomiting.pdf - rEMERGs
Vomiting.pdf - rEMERGs
Vomiting.pdf - rEMERGs
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VOMITING<br />
PATHOPHYSIOLOGY<br />
<strong>Vomiting</strong> center (VC)<br />
‣ Medulla, lateral reticular formation<br />
‣ Right beside centers for respiratory and salivary control<br />
‣ Ablation of vomiting center ----------> cannot vomit<br />
‣ Acts as coordinator of vomiting<br />
‣ Has direct input from gut sensors<br />
‣ Efferent nerves travel to diaphragm by phrenic nerve, to the stomach and<br />
small intestine by the vagus nerve, and to the abdominal muscles by<br />
spinal nerves<br />
Chemoreceptor Trigger Zone (CTZ)<br />
‣ Fourth Ventricle, in the area postrema, adjacent to vomiting center<br />
‣ Lies outside the blood - brain barrier and responds to circulating<br />
substances<br />
‣ Acts as an afferent relay station by receiving information from the gut<br />
(vagus)<br />
‣ Has direct connection to the vomiting center<br />
<strong>Vomiting</strong><br />
‣ Variety of stimuli; final common pathway is vomiting center<br />
‣ Emetic stimuli can originate from blood or virtually any organ<br />
‣ Three stages of vomiting ...<br />
nausea: hypersalivation and tacchycardia accompany<br />
wretching: spasmotic respiratory mvmts against closed<br />
glottis that moves stomach contents into lower esoph;<br />
bradycardia<br />
emesis<br />
PHARMACOLOGY<br />
Four mechanisms of action of anti-emetics<br />
‣ Depression of vomiting center<br />
‣ Depression of CTZ<br />
‣ Inhibition of input from vestibular apparatus to CTZ<br />
‣ Inhibition of input from peripheral receptors to VC<br />
Receptors<br />
‣ Dopaminergic: many dopamine receptors in the area postrema:<br />
haloperidol, metoclopramide, domperidone, phenothiazines<br />
‣ Histaminergic (H1) and cholinergic: receptors occur in the lateral<br />
vestibular nucleus and nucleus ambiguus: antihistamines<br />
(diphenhydramine, scopoloamine, promethazine) useful for motion<br />
sickness<br />
‣ Serotonergic (5HT): important neurotransmitter centrally in the area<br />
postrema and peripherally in the intestine thus antagonists are useful<br />
(ondansetron, granisetron)<br />
CLINICAL FEATURES<br />
Differential Diagnosis<br />
‣ Box 15-1: causes of acute N/V
‣ History and physical findings are the key to narrow the ddx<br />
Complications<br />
‣ Dehydration: loss of gastric contents + renal loss of Na+/Bicarbonate; ie,<br />
increased delivery of sodium bicarbonate to distal tubule and not all can<br />
be reabsorbed thus some Na+/Bicarb lost in urine<br />
‣ Metabolic alkalosis (Chloride responsive): loss of Hcl in vomitus<br />
‣ Hypokalemia: mostly renal loss with increased exchange of Na+ and K+<br />
although K+ in emesis does contribute<br />
‣ Mallory - Weiss tear: UGI bleeding<br />
‣ Esophageal perforation<br />
‣ Gastric rupture<br />
‣ Esophageal bleeding<br />
Investigations<br />
‣ Depends on hx and physical examination<br />
‣ AXR with suspected obstruction, perforation, gastric outlet obstruction<br />
‣<br />
‣<br />
‣<br />
Management<br />
‣<br />
‣<br />
‣<br />
‣<br />
‣<br />
CXR with suspected pneumonia in children<br />
Lytes, BUN, Cr only needed with protracted vomiting or signs of<br />
dehydration: classic result is a hypokalemic, hypochloremic metabolic<br />
alkalosis<br />
CBC rarely helpful<br />
Rehydration as needed<br />
NG or OG tube for gastric outlet obstruction or bowel obstruction<br />
Antiemetics: NOTE that anticholinergics are contraindicated in patients<br />
with gastric outlet obstruction or gastric retention (think of gastric outlet<br />
obstruction in patient with chronic ulcer disease)<br />
Prochorperazine: relatively contraindicated in pediatric population<br />
because of increased incidence of extrapyramidal side-effects<br />
Further investigation, management, and disposition depends on working<br />
dx
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