Acute ischemic colitis secondary to air embolism after diving

Abstract

Ischemic colitis (IC) secondary to air embolism from decompression sickness or barotrauma during diving is an extremely rare condition. After extensive review of the available literature, we found that there has been only one reported case of IC secondary to air embolism from diving. Although air embolization from diving and the various medical complications that follow have been well documented, the clinical manifestation of IC from an air embolism during diving is very rare and thus far unstudied. Common symptoms of IC include abdominal pain, bloody or non-bloody diarrhea or nausea or vomiting or any combination. Emergency physicians and Critical Care specialists should consider IC as a potential diagnosis for a patient with the above-mentioned symptoms and a history of recent diving. We report a case of IC from air embolism after a routine dive to 75 feet below sea level in a 53-year-old White female who presented to a community Emergency Department complaining of a 2-day history of diffuse abdominal pain and nausea. She was diagnosed by colonoscopy with biopsies and treated conservatively with antibiotics, bowel rest, and a slow advancement in diet.

INTRODUCTION

Ischemic colitis (IC) results from a reduction in blood flow through the mesenteric vasculature. Several mechanisms can lead to acute IC. Of the mechanisms resulting in acute IC, however, air embolism from diving is exceedingly rare.

Pulmonary barotrauma or decompression sickness during the dive can cause gas bubbles to form, which then may embolize into the systemic circulation and produce ischemia in organs with poor collateral circulation. These air embolisms can damage the pulmonary, cutaneous, musculoskeletal, and lymphatic systems, and can be deadly when they enter the cerebral or coronary arteries.[1] Common post-dive gastrointestinal (GI) complaints include abdominal pain, nausea, and vomiting. During descent, patients may swallow large quantities of air, which remains trapped in the stomach because they are unable to release it by the process of belching.[2] If this trapped air in the stomach is not released, it can expand during ascent and lead to significant GI manifestations including gastric or diaphragmatic rupture.[3,4] Other GI complications such as variceal bleeding and mesenteric venous thrombosis are also exceedingly rare, but have been reported in the literature.[5,6]

The result of IC from air embolism post-dive has only been reported once in which the patient presented with typical symptoms of IC, namely, abdominal pain and bloody diarrhea.[7] The diagnosis of IC is based on collected data from physical exam, laboratory data, radiological studies, and endoscopic findings with biopsies along with a high clinical suspicion. Treatment of either conservative therapy or surgical management is determined by the degree of physical, laboratory, and radiological findings, as well as, severity of symptoms. We present our patient's case below.

CASE REPORT

A 53-year-old White female presented to the Emergency Department (ED) with a chief complaint of diffuse abdominal pain and nausea for the last 3 days. The patient stated she was an experienced diver and that 4 days prior was on vacation and went diving for 30 minutes to a depth of 75 feet each day. During one of her excursions, she surfaced 1 minute early and had to dive back down and resurface again to avoid decompression sickness. Once on the boat, the patient only complained of feeling lightheaded. That evening around 10 p.m., she began experiencing severe diffuse lower abdominal pain and nausea. The next day, she complained of the same abdominal pain, which had relented slightly, but now accompanied by nausea and a temperature of 101.2΀F. The following day, she had the same abdominal pain, which was again severe and now localized primarily in the right lower quadrant. The patient was concerned she may have appendicitis and came to the ED. A review of systems was negative for diarrhea, blood in the stool, or vomiting over the last 3 days.

The patient denied any medical problems and was not on any medication. Her prior surgical history included tubal ligation and parathyroidectomy.

Upon physical exam, the patient was normotensive and afebrile with a heart rate of 67 beats per minute (BPM) and 18 respirations per minute. She appeared to be in minor distress secondary to the abdominal pain, but was alert, oriented, and pleasant. The lungs were clear bilaterally and the heart was regular without murmurs. The abdomen was mildly distended with diminished bowel sounds. There was exquisite tenderness throughout the lower abdomen with the right lower quadrant being the tenderest area. There was mild guarding along with mild rebound tenderness. The rectal exam was normal with brown stool grossly negative for blood, but hemoccult positive.

Initial labs were positive for a white blood cell count of 13.4 K/microliter with 80% neutrophils and 14% lymphocytes. Hemoglobin, hematocrit, urinalysis, and complete metabolic panel were all within normal limits.

A computed tomography (CT) scan of the abdomen and pelvis with and without intravenous and oral contrast demonstrated a short segment of bowel involving the cecum with marked bowel wall thickening and normal appearing appendix [Figure 1]. There was no free air, free fluid, or pelvic lymphadenopathy.

Figure 1.

(a) CT scan of the abdomen and pelvis with intravenous and oral contrast demonstrated a short segment of bowel involving the cecum with marked bowel wall thickening and normal appearing appendix. There was no free air, free fluid, or pelvic lymphadenopathy. (b) CT scan of the abdomen and pelvis with intravenous and oral contrast demonstrated a short segment of bowel involving the cecum with marked bowel wall thickening and normal appearing appendix. There was no free air, free fl uid, or pelvic lymphadenopathy

The patient was medically resuscitated with intravenous fluids and morphine for analgesia. However, because she was still having acute attacks of breakthrough pain that were 10 out of 10, hydromorphone was added to her regimen and this was ultimately effective in controlling her pain. She was also given ondansetron as needed for nausea and started on empiric antibiotics. The patient was admitted to the medical/surgical floor of the hospital and made NPO status. The patient was evaluated by gastroenterology and scheduled her for colonoscopy in the morning.

A colonoscopy revealed edematous mucosa, erythema, and superficial ulcerations without bleeding at the level of the mid ascending colon at about 65 cm from the anal verge [Figure 2]. Two superficial biopsies were taken which showed essentially architecturally unremarkable colonic mucosa with acute inflammatory cells in the lamina propria, focal erosion, and fibrinopurulent exudation with a differential diagnosis of IC versus pseudomembranous colitis [Figure 3].

Figure 2.

Images of colonoscopy. At the level of the mid ascending colon, at about 65 cm, there are typical changes in the mucosa of edema, erythema, and superficial ulcerations. No significant bleeding

Figure 3.

Pathology: (a) slide 1. Essentially architecturally unremarkable colonic mucosa with acute inflammatory cells in the lamina propria, focal erosion, and fibrinopurulent exudation. Considerations include ischemic colitis. (b) Slide 2. Essentially architecturally unremarkable colonic mucosa with acute inflammatory cells in the lamina propria, focal erosion, and fibrinopurulent exudation. Considerations include ischemic colitis. (c) Slide 3. Essentially architecturally unremarkable colonic mucosa with acute inflammatory cells in the lamina propria, focal erosion, and fibrinopurulent exudation. Considerations include ischemic colitis. (d) Slide 4. Essentially architecturally unremarkable colonic mucosa with acute inflammatory cells in the lamina propria, focal erosion, and fibrinopurulent exudation. Considerations include ischemic colitis

After reviewing all of the available data, the patient was diagnosed with acute IC secondary to air embolism from decompression sickness after diving. She was treated conservatively with IV fluids, pipercillin/tazobactam and morphine and was monitored closely for signs of decompensation with serial abdominal exams. She remained afebrile for the duration of her hospital stay and her diet was slowly advanced to regular. Daily complete metabolic panels were drawn and showed insignificant changes in electrolytes. On hospital day 3, her WBC normalized to 7.8 × 10³/microliter and continued to decrease. She was discharged home on hospital day 5 on a regular diet, free of abdominal pain, and given a prescription for ciprofloxacin and metronidazole, and instructed to follow-up with her primary care doctor. The patient followed up with her primary doctor 1 week, 1 month, and 6 months after discharge and remained free of abdominal pain or any other complaints associated with the diving incident.

DISCUSSION

Self-contained underwater breathing apparatus (SCUBA) diving is a popular sport with several million certified divers in the United States alone.[8] The two most well-known complications of diving are barotrauma and decompression sickness.

Barotrauma is the most common complication of diving and is a product of Boyle's law, (P1V1 = P2V2), which states that at a constant temperature, the volume of gas varies inversely with the pressure to which it is subjected.[1] For a diver, this means that the volume of gas confined in body cavities such as the lungs, ear, sinuses, and bowel will contract as ambient pressure increases during decent of the dive and will subsequently expand upon ascent. This can lead to multiple complications including tissue edema, alveolar or bowel rupture, or hemorrhage if the surrounding tissues do not adequately adapt. If alveolae rupture from overdistention along with concomitant vascular tear, gas may enter systemic circulation which can then embolize to multiple sites. The most common clinical manifestations result from gas emboli to the brain which can occur on ascent and produce syncope.[9]

Decompression sickness is explained by Henry's law (V = K × P) which states that the volume of a dissolved inert gas in a volume of liquid is directly proportional to the partial pressure of that gas in equilibrium within that liquid. After a diver has descended and is breathing air from the SCUBA tank, which contains nitrogen, the solubility of nitrogen will be increased leading to a larger amount dissolved in both body fluids and tissues.[7] Because nitrogen is five times more soluble in fat than in water, its removal from tissue may take hours.[7] If a diver ascends to the surface too quickly, the partial pressure of the gases saturated in the tissue may exceed the ambient pressure, leading to formation of bubbles which can enter into circulation.[1] The most common symptoms of localized pain, numbness/paresthesia, and muscular weakness typically present within the first 24 hours, while symptoms of gas embolism from pulmonary barotrauma occur immediately upon ascent[9,10] [Tables 1 and 2]. Because subtle symptoms of pulmonary barotrauma may not be recognized until hours later, timing of symptoms should not become the only criterion for distinguishing barotrauma from decompression sickness.[9]

Table 1.

Frequency of decompression sickness symptoms in 935 cases

Table 2.

Time to onset of decompression sickness after diving

The formed gas bubbles can enter the systemic arterial circulation by four suspected mechanisms: passage into pulmonary veins, directly into arterial circulation, large quantities of gas that cannot be fully filtered by pulmonary capillaries, or emboli that enter venous circulation and pass through a right-to-left shunt, such as a patent foramen ovale.[1,7] Arterial gas embolization is the second most common cause of death to divers, with sequela dependent on the final destination of the emboli with mortality rate from 7 to 14%.[7,9]

Experimental conditions have shown that bowel ischemia does not occur until the perfusion pressure is reduced to 30 mmHg or the mean arterial pressure of the mesentery is reduced to 45 mmHg.[11] Traditionally, the most common presenting complaints of IC are acute severe abdominal pain out of proportion to the physical exam, along with possible nausea, vomiting, diarrhea, or bloody stools.[12] As these patients present to the ED, they are typically worked up with laboratory blood work and CT of the abdomen and pelvis. Although no pathognomonic laboratory test exists for colonic ischemia, increased serum lactate dehydrogenase (LDH), lactic acid, creatine phosphokinase (CPK), or amylase, with a white blood cell count above 20 K/uL along with metabolic acidosis should highly increase suspicion of IC[13] [Table 3].

Table 3.

Laboratory, EKG, Radiographic, and Hemodynamic findings associated with air emboli

Gas bubbles formed from pulmonary barotrauma or decompression sickness can embolize to multiple sites in the body, which can result in ischemia to several organ systems and cause a variety of symptoms and physical findings. Table 4 shows the differential diagnosis of air embolism. Although no diagnostic blood test exists for air embolism, one study showed that widespread gas embolization resulted in markedly elevated serum creatine kinase with some values greater than 900 U/L.[14] Both the MM and MB components were found to be elevated, with the MM fraction being the predominant isoenzyme. The elevated CK reflected damage to tissues and organs with higher CK levels indicating greater amounts of muscle injury.[14] Higher levels of CK were found to be a negative clinical indicator of outcome.[14]

Table 4.

Differential diagnosis of air embolism

The CT findings of bowel wall thickening, pericolic fat stranding, and “thumb printing” are suggestive, but nonspecific, for IC.[15,16] The findings of pneumatosis intestinalis and mesenteric or portal venous gas are more suggestive of IC, but are usually late signs and occur infrequently.[15]

Clinically stable patients suspected of IC typically undergo further evaluation with colonoscopy for definitive diagnosis. One hour of hypoxia can cause detectable injury to the inner mucosal layer of the bowel, while ischemia lasting between 8 and 16 hours leads to transmural infarction and necrosis.[17] The most common visual findings from endoscopy were petechial hemorrhages, edematous or fragile mucosa, scattered erosion, longitudinal ulcerations, and sharply defined erythematous segment of involvement.[18] A single linear ulcer seen on colonoscopy running along the longitudinal axis of the colon represents the "single-stripe sign" of IC.[19] Colonoscopy can be a great benefit for diagnosis because it also permits biopsies to be obtained.

The typical pathologic characteristics of IC are mucosal inflammation accompanied by erosion, granulation tissue hyperplasia and gland atrophy, lamina propria hemorrhage, and macrophages with hemosiderin pigmentation in submucosa in particular.[18] Our comparison report of IC caused by air embolism noted pathologic findings of air in the lamina propria.[7] There are three broad causes, which encompass several disease processes, that may lead to air in the lamina propria, or pneumatosis coli, which include pulmonary disease, necrotic gastrointestinal disease, and any condition that increases the intraluminal pressure within the bowel. Although there is minimal available information regarding IC secondary to air embolism, we believe that the pathologic finding of pneumatosis coli, with a history of recent dive, should represent air embolism as the cause until proven otherwise.

Exploratory laparotomy is considered the gold standard for both diagnosis and subsequent treatment of unstable patients suspected of acute occlusive mesenteric ischemia with clinical decompensation or peritonitis.[12] Most patients who are hospitalized with IC do not require such invasive treatment and are instead treated conservatively with bowel rest, IV fluid resuscitation, and broad-spectrum antibiotics. IV fluid is imperative to restore intravascular volume and maximize oxygen delivery to the bowel. A nasogastric tube should be placed if the patient has an ileus or intractable vomiting. Empiric broad-spectrum antibiotics are given to cover aerobic and anaerobic bacteria to prevent sepsis from bacterial translocation after loss of mucosal integrity.[20] Patients are monitored closely with vital signs, daily blood work, frequent abdominal exams, and serial radiographic exams. We must note that due to the uniqueness of our case there has not been a reported case in which a patient suffering from IC secondary to air embolism after diving has deteriorated to the extent in which surgical management was necessary. However, we suggest that the standard recommendations for surgical intervention be applied in this unique scenario as well. An emergent exploratory laparotomy may be necessary if the patient begins having peritoneal signs, massive bleeding, and fulminant IC.[21] If symptoms persist for more than 2 or 3 weeks, or malnutrition or hypoalbuminemia due to protein-losing colonopathy occurs, a scheduled exploratory laparotomy is indicated.[21] Most patients with IC have resolution of their symptoms within 1–2 days and endoscopic and radiographic signs disappear by 2 weeks.[20]

Both our patient and our comparison case[7] were treated conservatively without the use of hyperbaric oxygen (HBO) therapy. Although there has yet to be a reported case in which HBO was used to treat IC as the result of air embolism from diving, we feel the need to mention its use as a potential acute or subacute treatment modality for future patients to be used at the discretion of the treating physician based on availability and patient condition. HBO is the primary treatment for both decompression sickness and arterial gas embolism.[22] HBO is defined by the Undersea and Hyperbaric Medical Society (UHMS) as a treatment in which a patient breathes 100% oxygen while the treatment chamber delivers a pressure greater than 1 atmosphere absolute (ATA).[23] The physiological effects of HBO are based on the gas laws of Boyle, Dalton, and Henry, as well as the biochemical effects of hyperoxia.[23] A patient breathing normobaric air with standard 21% oxygen will achieve an arterial oxygen tension of 100 mmHg with a tissue oxygen tension of approximately 55 mmHg with a plasma oxygen concentration of 3 mL/L.[23,24] HBO therapy will deliver 100% oxygen under 3 ATA. This affects the patient in several ways. The oxygen dissolved in plasma approaches 60 mL/L, which is sufficient to support resting tissue without contribution from hemoglobin.[23,24] Based on Boyle's law, the volume of any bubbles in plasma and tissue will be reduced by two thirds.[24] Due to the increased partial pressure of oxygen, the inert gas in the bubble will be replaced with oxygen, which will then be easily metabolized by the tissues.[23,24] There are limited data from clinical trials on HBO therapy versus no HBO therapy for air embolism, as HBO has been accepted as the only life-saving treatment for air embolism.[23] Treatment should begin as soon as possible with 100% at 2.8 ATA for 2–4 hours until resolution of symptoms up to 10 treatments.[22–24] Although HBO therapy has not been reported for the treatment of air embolism to the bowel, there are multiple articles published which demonstrate the usefulness of HBO treatment for cerebral artery air embolism.

One study evaluating HBO therapy for iatrogenic air embolism showed a reduction in mortality from 30 to 6% when patients were treated with HBO.[25] Although treatment with HBO is recommended as soon as possible, a time frame has not been established which showed that HBO was no longer indicated or useful after a certain amount of time. HBO was found to be effective in treating patients with cerebral air embolism in up to 60 hours after initial diagnosis.[26]

CONCLUSION

Air embolism resulting from decompression sickness or pulmonary barotrauma during diving can affect various tissues and organ systems and can be catastrophic if it enters cerebral or coronary circulation. The sequela of IC from air embolism secondary to diving is exceedingly rare with only one other reported case.[7] Both our case and our comparison case presented with complaints consistent with IC and were diagnosed with complete blood cell count, complete metabolic panel,,, CT scan, and colonoscopy with biopsies. Treatment is based on severity of symptoms and the patient condition and includes either conservative management or surgical intervention. Although there has not been a reported case of IC secondary to air embolism from diving subsequently treated with HBO therapy, we have mentioned this as a potential therapeutic modality to be used at the discretion of the physician.