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UHM 2002, Vol. 29, No. 4 – Diver with type II DCS
Diver with acute abdominal pain, right leg
paresthesias and weakness: A case report
J.WANG, K.CORSON, K. MINKY, J. MADER
Division of Hyperbaric Medicine and Wound Care
Department of Orthopedics and Rehabilitation
University of Texas Medical Branch, Galveston, Texas
Wang J, Corson K, Minky K, Mader J, A diver with type II decompression sickness and acute
appendicitis: A case report. Undersea Hyperb Med 2002; 29(4): 242-246 - A 29-year-old man was
brought to an emergency department by the United States Coast Guard with chief complaints of severe
abdominal pain, right leg paresthesia and weakness following four deep air dives. Physical examination
before recompression treatment was remarkable for diffuse abdominal tenderness and right leg weakness.
The patient was diagnosed in the emergency room with type II decompression sickness (DCS) and
underwent standard recompression therapy. He experienced complete resolution of weakness after
hyperbaric oxygen (HBO) therapy, but his abdominal pain was persistent. Further investigation led to the
diagnosis of acute appendicitis with perforation. The patient underwent appendectomy and intravenous
antibiotic therapy and was discharged to his home on hospital day five without complications. This case
reinforces the importance of careful clinical assessment of divers and illustrates the potentially wide
differential diagnosis of DCS. This is the first reported case of recompression treatment of a diver with
acute appendicitis and type II DCS.
DCS, HBO2, diver, abdominal pain, paresthesias, appendectomy
INTRODUCTION
Recreational scuba diving has become a popular sport in the United States, with almost
9 million certified divers. DCS is an uncommon condition, but poses a serious risk of scuba
diving with potential significant morbidity and mortality (1). Diagnosis of DCS can be difficult
because the presentation is often nonspecific. We report a case of a 29 year-old white male who
presented with severe abdominal pain, right leg paresthesia and weakness following four deep air
dives. The patient was initially diagnosed with possible DCS and treated with hyperbaric oxygen
(HBO) therapy. After closely following the patient’s clinical course, a perforated appendix was
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UHM 2002, Vol. 29, No. 4 – Diver with Type II DCS
also suspected. The patient underwent emergency laparotomy where intra-operative findings
demonstrated a suppurative gangrenous appendix and grossly purulent fluid in the peritoneum.
He was treated with intravenous antibiotics, and recovered fully without any complications.
CASE REPORT
A 29-year-old white male was brought to a university hospital emergency room by
helicopter with acute onset of abdominal pain, right leg paresthesia and weakness following four
deep air dives. He had been in his usual state of heath, and he was in the second day of a diving
trip. His dive profiles on the day of admission were: 92ft /34min; 82ft/40min; 74ft/20min;
72ft/25min. Twenty minutes after his last dive, the patient developed sudden right leg numbness,
tingling, weakness and epigastric pain. The abdominal pain was associated with nausea and
vomiting, and became progressively worse over the subsequent three hours. Investigation
indicated that the patient had approximately 67 minutes of omitted decompression on the last
four deep air dives. He was started on oxygen immediately and flown by the Coast Guard to the
hospital. At the time of arrival, he was alert and oriented, he complained of right leg weakness
and abdominal pain, however, the numbness, tingling sensation in his right leg reported earlier
had resolved. He denied fever or chills, had no change of vision, and no chest pain or shortness
of breath, or muscle or joint pain. The past medical history was only significant for hypospadias,
for which he underwent surgical repair as a child. Physical examination revealed a wellnourished, well-developed white male. He was alert and oriented, apparently in acute distress.
Blood pressure was 130/78 mmHg, pulse 87 beats per minute, respiratory rate 28 per minute, and
temperature 37°C. The mucous membranes appeared dry, and no skin rash, ecchymosis, or
lymphadenopathy was found. The chest was clear to auscultation and his heart had a regular
sinus rate and rhythm without murmur. The abdomen was soft, tender to palpitation diffusely,
but no guard and rebound; his bowel sounds appeared hypoactive. The scrotal area showed mild
erythema and was tender upon palpation and rectal tone was normal.
A neurological examination at emergency room showed his cranial nerves were grossly
intact, sensation including light touch, vibration and position were intact. Mild weakness was
noted in right lower extremity, with a motor strength III-IV/V. Deep tendon reflexes were
slightly hyperactive in the right lower extremity. The Romberg test, finger to nose and Babinski
sign were negative.
A chest x-ray at emergency room showed his lungs were clear and a plain film of the
abdomen showed no free air or dilated loops. An electrocardiogram showed a normal sinus rate
and rhythm. Other laboratory findings showed a white blood cell count of 22,000/mm3 with
granulocytes 88%, lymphocytes 4.4%, monocytes 7.7%, eosinophils 0.3%, basophils 0.3%.
Blood hemoglobin was 16.5 g/dl, hematocrit 46%, platelet 187/µl. Serum sodium was137mEq/l,
potassium 4mEq/l, chloride 99 mEq/l, bicarbonate 24 mEq/l, BUN 15 mg/dl, creatinine 0.87
mg/dl, serum glucose 122 mg/dl, alkaline phosphatase 103 u/l, aspartate aminotransferase (AST)
45 u /l, alanine aminotransferase (ALT) 46 u/l, gamma-glutamyltransferase (γ-GGT) 25 u /l,
lactatedehydrogenase (LDH) 844 u/l, amylase 57 u/l, lipase 35 u/l, total protein 8.2 mg/dl,
albumin 4.8mg/dl, total bilirubin 0.7 mg/dl, troponin T (TnT) <0.01 µg/l, creatine kinase (CK)
288 u/l, creatine kinase isoenzyme MB (CK-MB) 7.1 u/l, CK-MB index 2.5, partial
thromboplastin (PT) 18 seconds, activated partial thromboplastin time (APTT) 38 seconds, and
international normalization ratio (INR) 1.8.
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A tentative diagnosis of Type II DCS was made on the basis of the patient’s neurological
symptoms, the timing of onset of symptoms, and the history of omitted decompression. The
patient was started on intravenous fluid and sent to the hyperbaric chamber for oxygen
recompression therapy. The patient was initially recompressed on a Comex 30 treatment table
using 50/50 N2/O2 at maximal depth and in accordance with the table at 60 fsw. The patient was
then switched to United States Navy (USN) Table 6. The patient reported a near complete
resolution of his right lower extremity weakness after 30 minutes of treatment, but continued
complaining of abdominal pain and vomited twice during the first 30 minutes of treatment.
Urinary retention was also noted during treatment and after catheterization 450ml of urine was
obtained and a sample sent for analysis. The abdominal pain persisted and gradually localized to
the right lower quadrant of his abdomen.
Physical examination performed immediately after completion of the HBO2 therapy
showed: blood pressure 170/100 mmHg, pulse 92 beats per minute, respiratory rate 29 per
minute, and temperature 37.8ºC. The patient’s abdomen became rigid with severe tenderness to
palpation in the lower abdomen. Along with maximal tenderness at McBurney’s point, rebound
tenderness was also present. Costovertebral angle tenderness was absent and a careful
neurological examination was normal.
General surgery was consulted and the patient taken to the operating room for
exploratory laparotomy. Intra-operative findings demonstrated suppurative gangrene of the
appendix and grossly purulent fluid in the peritoneum. Appendectomy was performed, the
peritoneal cavity was carefully irrigated, and a drain left in place. Culture of the peritoneal fluid
yielded Citrobacter Pfreundii, and histopathology confirmed acute transmural appendicitis and
peri-appendicitis. The patient was treated with intravenous antibiotics postoperatively and
discharged to home on hospital day six without complications.
DISCUSSION
Serious decompression injuries can be life-threatening incidents. DCS may be classified
into Type I (mild or pain only) and Type II (serious or neurological) (1). Neurological symptoms
or signs beginning after diving require immediate investigation for DCS and delays in diagnosis
are undesirable due to the potentially progressive nature of the condition. The most common
presenting symptoms in type II DCS are sensory findings such as paresthesias and limb
weakness. Abdominal and lower back pain are encountered in spinal cord DCS (3). Abdominal
pain in diving also has been reported in abdominal barotrauma causing rupture of stomach (6,7),
intestine (8), and diaphragm (9,10). Mesenteric venous thrombosis following diving (11) can
also present as abdominal pain. Pathophysiological events in DCS predispose to vascular
obstruction and venous infarction (12,13).
The diagnosis of DCS can be challenging since the presentation of DCS is variable and
nonspecific, and there are no diagnostic tests currently available other than clinical response to
recompression. The urgent nature of the problem demands rapid clinical assessment and
decision-making; misdiagnosis or delay in recompression may lead to poor clinical outcome,
especially in cases of type II DCS. Other medical conditions can also mimic or co-exist with
DCS. Butler (16) reported a case in which an initial evaluation considered musculoskeletal DCS,
but a pneumothorax was identified and successfully treated without sequelae. Siermonwski et al
(17) presented a diver with viral infection masking DCS and another diver with DCS
misdiagnosed as viral infection. Beckman (18) reported a diver initially diagnosed as having
type II DCS who was later found to have viral meningitis. Vasculitis masquerading as
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neurological DCS has also been reported (19). A diver who became unconscious after
gastroenteritis was diagnosed as having DCS, but subsequent investigations revealed mental
status changes resulting from maple syrup urine disease (partial-chain ketoacid decarboxylase
deficiency) (20). Appendicitis co-presenting with DCS has not been reported previously.
In our case, a diagnosis of DCS was initially made based on the patient’s presenting
symptoms and signs (right leg paresthesia, weakness pain, along with abdominal pain and
dysfunction of the bladder), timing of onset of symptoms (twenty minutes after diving), risk
factors (multiple dives and dehydration), and omission of decompression (approximately 67
minutes during four deep air dives). Carefully observing the progress of clinical signs of
abdominal pain during and after HBO treatment shifted attention to the second diagnosis of acute
abdomen. The patient underwent emergency appendectomy, was treated with intravenous
antibiotics, and recovered fully without complications. The case reinforces the importance of
differential diagnosis of neurological DCS, especially when primary treatment with oxygen
recompression tables is not completely successful. To our knowledge, our case is the first report
of recompression treatment of a diver with type II DCS and acute appendicitis.
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