CRITICAL CARE M

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CRITICAL CARE MM

• Adam Noyes PGY-3
• Justin Goralnik PGY-2

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Cause of Death

• Hydrochloric Acid Ingestion
• pH 1
• It is a highly corrosive, strong mineral acid
  with many industrial uses (household cleaning).
• Hydrochloric acid is found naturally in gastric
  acid.

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Caustic Ingestions

• The clinical features of caustic ingestions vary
  widely.
• Early signs and symptoms may not correlate with
  the severity and extent of tissue injury.
• Patients may complain of oropharyngeal,
  retrosternal or epigastric pain,
  dysphagia/odynophagia, or hypersalivation.
• Persistent severe retrosternal or back pain may
  indicate esophageal perforation with
  mediastinitis.
• Other findings include vomiting, hematemesis, and
  persistent, localized abd tenderness, rebound,
  and rigidity that may indicate esophageal or
  gastric perforation with peritonitis.
• Caustic injury to the oropharynx causes pain and
  inability to clear pharyngeal secretions with
  persistent drooling.
• Hoarseness, stridor, aphonia and respiratory
  difficulties are less common and result from
  caustic burns of the epiglottis and larynx.
• Fever, tachycardia, and shock generally imply the
  presence of more severe and extensive injury.

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Caustic Ingestions

• Alkali ingestions damage the esophagus more than
  the stomach or duodenum.
• Either acid or alkali can also induce both
  laryngeal and tracheobronchial injury.
• Acids cause more severe gastric injury.
• In contrast to the more viscous alkaline
  solutions, acid preparations tend to pass quickly
  into the stomach, causing less esophageal damage.

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Caustic Ingestion

• Acid ingestion produces a superficial coagulation
  necrosis that thromboses the underlying mucosal
  blood vessels and consolidates the connective
  tissue forming an eschar.
• Because acid solutions cause pain upon contact
  with the oropharynx, the amount of acid ingested
  tends to be limited.

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HCl Necrosis
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Acids and Bases

• A study comparing outcomes of acid or alkali
  ingestion found that outcomes were overall worse
  for those who ingested acid.
• Such patients had significantly more severe
  mucosal injury, were more likely to be
  hospitalized in the ICU, have systemic
  complications or perforation, and had higher
  mortality.

Poley JW, Gastrointest Endosc. 200460(3)372.
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Pathologic Severity of Injury

•  Caustic injuries to the gastrointestinal tract
  are classified pathologically, similar to burns
  of the skin
• First-degree injury results from superficial
  mucosal damage and is characterized by focal or
  diffuse erythema, edema, and hemorrhage. No scar
  formation.
• Second-degree injury shows mucosal and
  sub-mucosal damage, ulcerations, exudates, and
  vesicle formation. Granulation tissue and then a
  fibroblastic reaction, produces a scar and
  possible stricture.
• Third-degree injury is transmural and is
  characterized by deep ulcers and black
  discoloration and perforation of the wall.

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Diagnosis and Staging

• Oropharynx may reveal edema, erosions, or deep
  necrosis with grayish pseudomembranes.
• Absence of oropharyngeal burns does not preclude
  the presence of esophageal or gastric injury.
  Thus, upper endoscopy should be performed during
  the first 24 hours after ingestion to evaluate
  esophageal and gastric damage, establish
  prognosis, and guide therapy.
• Endoscopy is contraindicated in patients who are
  hemodynamically unstable, have evidence of
  perforation, or exhibit severe oropharyngeal or
  glottic edema and necrosis.

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Endoscopy
Endoscopy demonstrated complete necrosis from the
hypopharynx to the pylorus. a Hypopharynx (upper
part tracheal tube). b Esophagus. c Gastric
corpus. d Gastric antrum.
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Diagnosis and Staging

• A grading system for esophageal injury to predict
  clinical outcome with corrosive ingestions.
• Grade 0 Normal
• Grade 1 Mucosal edema and hyperemia
• Grade 2A Superficial ulcers, bleeding, exudates
• Grade 2B Deep focal or circumferential ulcers
• Grade 3A Focal necrosis
• Grade 3B Extensive necrosis

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Staging and Prognosis

• The following correlations between endoscopic
  grading and prognosis have been observed
• Patients with grades 1 and 2A have an excellent
  prognosis without significant acute morbidity or
  subsequent stricture formation.
• Patients with grades 2B and 3A develop strictures
  in 70-100 of cases.
• Grade 3B carries a 65 early mortality and the
  need for esophageal resection in most cases.

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Staging and Prognosis

• Mucosal injury grade 3 is associated with a high
  rate of systemic complications including bleeding
  and perforation.
• In a large retrospective study, patients with
  grade 3B mucosal injuries were at greater risk of
  prolonged hospital stay (OR 2.4), ICU admission
  (OR 10.8), and gastrointestinal and systemic
  complications (OR 4.2 and 4.1, respectively).
• Mortality of patients with one or more systemic
  complications was considerably high (45). Dalus
  et al. reported a 100 mortality in patients with
  perforation or orotracheal fistula.

Cheng HT, BMC Gastroenterol. 2008831.
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Management

• Patients suspected of having significant
  ingestions (based on history, symptoms, or
  endoscopic findings of grade 2B or greater
  injury) should generally be treated in a surgical
  or medical intensive care unit in order to manage
  the acute, life-threatening complications of
  injury (mediastinitis, peritonitis, respiratory
  distress, shock) and to decrease the risk of
  developing late esophageal strictures.
• Endoscopy should be performed as soon as
  possible, ideally within 24 hours, in order to
  assess the magnitude and extent of injury.

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Management

• If the epiglottis or the larynx is edematous,
  endotracheal intubation is contraindicated and a
  tracheostomy should be performed for airway
  control.

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Management

• Grade 2b3b injuries have a high risk to develop
  post-acute strictures and should be treated by
  early endoscopic dilatation.
• Robustelli et al. suggested to perform CT scan in
  every patient with endoscopic grade 3 burn to
  detect early signs of perforation.
• Prophylactic antibiotic therapy is generally
  recommended.

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Management

• Esophagectomy may be required for patients with
  severe strictures.
• The need to perform surgery for caustic injuries
  has a persistent long-term negative impact on
  survival and functional outcome.
• In addition, clinical signs of perforation,
  mediastinitis, or peritonitis are indications for
  emergency surgery.

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Management

• It is also important to recognize that certain
  agents and procedures are contraindicated in the
  presence of caustic ingestions
• Use of emetics is contraindicated because
  vomiting re-exposes the esophagus and the
  oropharynx to the caustic agent, further
  aggravating injury.
• Neutralizing agents (weakly acidic or basic
  substances) should not be administered because
  damage is generally instantaneous. Furthermore,
  neutralization releases heat that adds thermal
  injury to the ongoing chemical destruction of
  tissue.
• Nasogastric intubation to remove any remaining
  caustic material is contraindicated because it
  may induce retching and vomiting which can
  compound injury and possibly lead to perforation
  of the weakened esophagus or stomach.

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Late Sequelae

• After resolution of the initial injury patients
  are at risk for developing esophageal strictures
  and esophageal squamous cell carcinomas.
• Up to one-third of patients who suffer caustic
  esophageal injury develop esophageal strictures,
  primarily in those with grade 2B or 3 injuries.
• The peak incidence of dysphagia due to esophageal
  stricture formation after corrosive esophageal
  injury is two months, although it can occur as
  early as two weeks or as late as years after
  ingestion.

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Late Sequelae

• The risk for development of esophageal squamous
  cell carcinoma is 1000-fold higher in victims of
  alkali ingestion compared to the general
  population (annual risk of 2.6 per 100,000).
• In one study of 63 patients, the mean latency
  period for development of esophageal cancer was
  41 years.
• Nearly all reported patients with corrosion
  carcinoma had consumed an alkali, although two of
  three patients in one study had consumed acid.
• The risk of gastric cancer does not appear to be
  increased.

Appelqvist P. Cancer. 198045(10)2655
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