Dolor abdominal

Abdominal Pain in Patients With Hyperglycemic Crises
Guillermo Umpierrez and Amado X. Freire

Background: The aim of the study was to evaluate the dosis. In DKA patients with abdominal pain, the mean
incidence and prognosis of abdominal pain in patients serum bicarbonate (9 ؎ 1 mmol/L) and blood pH
with diabetic ketoacidosis (DKA) and hyperglycemic (7.12 ؎ 0.02) were lower than in patients without pain
hyperosmolar nonketotic state (HHS). Abdominal (15 ؎ 1 mmol/L and 7.24 ؎ 0.09, respectively, both
pain, sometimes mimicking an acute abdomen, is a P Ͻ .001). Abdominal pain was present in 86% of pa-
frequent manifestation in patients with DKA. The tients with serum bicarbonate less than 5 mmol/L, in
prevalence and clinical significance of gastrointestinal 66% of patients with levels of 5 to less than 10
symptoms including abdominal pain in HHS have not mmol/L, in 36% of patients with levels 10 to less than
been prospectively evaluated. 15 mmol/L, and in 13% of patients with bicarbonate
Materials and Methods: This is a prospectively col- levels 15 to 18 mmol/L. Patients with DKA and ab-
lected evaluation of 200 consecutive patients with hy- dominal pain had a more frequent history of alcohol
perglycemic crises admitted to a large inner-city teach- (51%) and cocaine abuse (13%) than those without ab-
ing hospital in Atlanta, GA.We analyzed the admission dominal pain (24% and 2%, respectively, both P Ͻ
clinical characteristics, laboratory studies, and hospi- .001). One patient with HHS reported nausea and vom-
tal course of 189 consecutive episodes of DKA and 11 iting on admission, but abdominal pain was not re-
cases of HHS during a 13-month period starting in ported in any patient with HHS.
October 1995. Conclusions: Gastrointestinal manifestations includ-
Results: Abdominal pain occurred in 86 of 189 pa- ing abdominal pain are common in patients with DKA
tients with DKA (46%). In 30 patients, the cause of ab- and are associated with severe metabolic acidosis and
dominal pain was considered to be secondary to the with a history of alcohol or cocaine abuse, but not
precipitating cause of metabolic decompensation. with the severity of hyperglycemia or dehydration. Our
Five of them required surgical intervention including study indicates that investigation of the etiology of
1 patient with Fournier’s necrotizing fasciitis, 1 with abdominal pain in DKA should be reserved for patients
cholecystitis, 1 with acute appendicitis, and 2 patients without severe metabolic acidosis or if the pain per-
with perineal abscess.The presence of abdominal pain sists after the resolution of ketoacidosis.
was not related to the severity of hyperglycemia or Copyright 2002, Elsevier Science (USA). All rights
dehydration; however, a strong association was ob- reserved.
served between abdominal pain and metabolic aci-

abdomen, is especially common in children.6,7
D IABETIC KETOACIDOSIS (DKA) and hy-
perglycemic hyperosmolar nonketotic state
(HHS) are the most common hyperglycemic emer-
These abdominal manifestations occur in 40% to
75% of cases of DKA.8-11 The abdominal pain usu-
gencies in patients with diabetes. It is estimated that ally resolves with correction of hyperglycemia,
DKA and HHS account for up to one fourth of all metabolic acidosis, and electrolyte disturbances.
diabetes-related hospital admissions,1-4 and recent However, in the face of such severe illness and be-
epidemiologic studies in the United States indicate cause of fear of missing an intra-abdominal med-
that hospitalizations for DKA and HHS are in- ical or surgical process that may have precipitated
creasing.1 Despite advances in their treatment, DKA the development of ketoacidosis, extensive labora-
and HHS remain serious events with mortality rates tory and radiologic studies may be ordered. In some
as high as 5% to 10%.2,5 The cause of death in pa- instances, exploratory laparotomy is performed
tients with DKA and HHS rarely results from the without positive results, increasing the cost of med-
metabolic complications of hyperglycemia or meta- ical care, and the morbidity and mortality risk in
bolic acidosis but relates to the underlying medical patients with DKA.12-14
illness that precipitated the ketoacidosis. Thus, suc-
cessful treatment requires a prompt and careful
search for the precipitating cause. From the Department of Medicine and Preventive Medicine,
The clinical presentation of DKA usually devel- University of Tennessee Health Science Center, Memphis, TN.
ops rapidly, over a time span of less than 24 hours. Address reprint requests to Guillermo E. Umpierrez, MD, As-
Polyuria, polydipsia, and weight loss may be pre- sociate Professor of Medicine, Department of Medicine, Uni-
versity of Tennessee Health Science Center, 951 Court Ave, Rm
sent for several days before the development of ke-
340M, Memphis, TN 38163.
toacidosis, whereas nausea, vomiting, and abdom- Copyright 2002, Elsevier Science (USA). All rights reserved.
inal pain are frequently the presenting symptoms. 0883-9441/02/1701-0009$35.00/0
Abdominal pain, sometimes mimicking an acute doi:10.1053/jcrc.2002.33030

Journal of Critical Care, Vol 17, No 1 (March), 2002: pp 63-67 63

64 UMPIERREZ AND FREIRE

Most patients who develop HHS do so over days RESULTS
to weeks, during which they have experienced The study population included 189 patients with
polyuria, polydipsia, and progressive decline in the DKA and 11 patients with HHS. Their clinical char-
level of consciousness. The most common reason acteristics are shown in Table 1. Abdominal pain
for seeking medical attention is unresponsive- was reported in 86 of 189 patients with DKA
ness.4,15 In patients with HHS, the prevalence of (46%). Patients with DKA and abdominal pain
gastrointestinal symptoms including abdominal were younger (37 Ϯ; 1 yr, standard error of mean)
pain has not been reported. than patients without abdominal pain (41 Ϯ 2 yr,
The aim of this study was to determine the preva- P ϭ .03). The mean duration of diabetes and num-
lence and clinical significance of abdominal pain ber of patients with newly diagnosed diabetes were
in patients with hyperglycemic crises. similar between DKA patients with and without ab-
dominal pain. Pain was associated with abdominal
MATERIALS AND METHODS tenderness in all patients, and rebound tenderness
This was a prospective evaluation of 200 consecutive patients was present in 12% of patients. Nausea and vom-
with hyperglycemic crises admitted to Grady Memorial Hos- iting were reported in 66% of DKA patients with
pital in Atlanta during a 13-month period starting in October abdominal pain and in 35% of patients without ab-
1995. Of the 200 patients, 189 patients (95%) met the diag- dominal pain (P Ͻ .001). No patient with HHS
nostic criteria for DKA (111 men and 82 women) and 11 pa-
complained of abdominal pain on admission and
tients were admitted with HHS (4 men and 7 women). The di-
agnosis of DKA was established in the emergency department
only 1 patient with HHS who had a known history
by a plasma glucose level greater than 13.8 mmol/L (250 of gastroparesis reported nausea and vomiting
mg/dL), a serum bicarbonate level lower than 15 mmol/L, a before admission.
blood pH less than 7.3, a calculated anion gap greater than 14 In 30 of the 86 DKA patients with abdominal
mmol/L, a positive serum ketone level at a dilution equal to or pain (35%), the etiology of the pain was consid-
greater than 1:4 by the nitroprusside reaction. Diagnostic crite-
ered to be secondary to the precipitating cause of
ria for HHS included a plasma glucose level greater than
600 mg/dL (33.3 mmol/L), a total serum osmolality greater than
metabolic decompensation. Four patients presented
320 mmol/kg, a blood pH greater than 7.3, a serum bicarbon- with acute pancreatitis and 4 with acute exacerba-
ate level greater than 15 mmol/L, and a serum ketone level equal tion of chronic alcoholic pancreatitis. Three pa-
to or less than 1:2 dilutions. Total serum osmolality was calcu- tients were diagnosed with acute alcoholic hepati-
lated as follows:

[2 ϫ sodium ion (mmol/L)] ϩ [glucose (mg/dL)/18]
ϩ [blood urea nitrogen (mg/dL)/2.8], Table 1. Clinical Characteristics on Admission

with normal values being 290 Ϯ 5 mmol/kg of water. DKA With DKA Without
Abdominal Pain Abdominal Pain
The presence or absence of abdominal pain, nausea, and vom-
iting was recorded on admission. The evidence of abdominal Number of patients 86 103
guarding and rebound tenderness was sought on physical ex- Age (yrs) 37 Ϯ 13 41 Ϯ 21
amination. In addition, patient information was collected re- Sex (men/women) 47/43 64/39
garding demographic characteristics, precipitating cause for Duration of diabetes (yr) 7Ϯ1 9Ϯ1
metabolic decompensation, substance abuse (alcohol or co- New-onset diabetes 16 (18) 18 (17)
caine), renal disease, previous history of DKA or HHS, glucose History of alcohol use 44 (51)† 25 (24)
and acid-base status, concurrent medical diagnoses, and hospi- History of cocaine use 11(13)‡ 2 (2)
tal outcome including mortality. Blood glucose (mg/dL) 596 Ϯ 246 586 Ϯ 245
Bicarbonate (mmol/L) †
9 Ϯ 1† 15 Ϯ 15
PH 7.12 Ϯ .02† 7.24 Ϯ .092
Statistical Analysis Sodium (mmol/L) 133 Ϯ 133 133 Ϯ 133
Comparisons of demographics and continuous clinical char- Potassium (mmol/L) 5.4 Ϯ 1‡. 5.0 Ϯ .10
acteristics between groups were performed by using unpaired Serum osmolality (mmol/L) 307 Ϯ 207 307 Ϯ 207
t test. For categoric variables, ␹2 analysis was used when ap- BUN (mg/dL) 24 Ϯ 24 24 Ϯ 22
plicable. Association between metabolic acidosis and severity Creatinine (mg/dL) 1.8 Ϯ .21 1.6 Ϯ .81
of abdominal pain was assessed by Mantel-Hanzel ␹2 analysis Data are means Ϯ SEM or n (%).
for trend in the 189 DKA patients. A P value of .05 was con- *P Ͻ .05.
sidered significant. StatView version 5.0 (SAS Institute, Cary, †
P Ͻ .0001.
NC) was the statistical software used for the analysis. ‡
P Ͻ .01.

ABDOMINAL PAIN IN DKA 65

tis, 2 with gastritis, 1 with peptic ulcer disease, and in 25 of the 29 (86%) patients with bicarbonate lev-
1 with viral hepatitis. Six patients had pyelonephri- els less than 5 mmol/L, in 66% of patients with lev-
tis, 2 had gastroenteritis, and 2 were considered to els between 5 and less than 10 mmol/L, in 36%
have pelvic inflammatory disease. Only 5 patients with levels 10 and less than 15 mmol/L, and in 13%
admitted with DKA and abdominal pain required of those with bicarbonate between 15 and 18
surgical intervention including 1 patient with mmol/L. The admission pH level also correlated
Fournier’s necrotizing fasciitis, 1 with cholecysti- with the presence of abdominal pain. A total of 86%
tis, 1 with acute appendicitis, and 2 with perineal of patients with pH less than 7.0 complained of ab-
abscess. dominal pain, a value higher than that reported in
We found no association between the presence patients with pH between 7 and less than 7.25 and
of abdominal pain and the initial blood glucose pH 7.25 to 7.30 in whom pain was 47% and 25%,
level and/or severity of dehydration as indicated by respectively, both P Ͻ .01.
the admission serum osmolality and urea nitrogen Noncompliance with medical therapy or discon-
concentration (Table 1). In contrast, we observed a tinuation of insulin was the leading cause of DKA
strong correlation between the severity of meta- and accounted for 57% of patients with abdominal
bolic acidosis and the presence of abdominal pain pain and 43% of patients without abdominal pain.
(P Ͻ .001). Patients with DKA and abdominal pain Substance abuse including alcohol and cocaine
had a mean serum bicarbonate (9 Ϯ 1 mmol/L) and abuse played an important role in decreased com-
blood pH level (7.12 Ϯ 0.02) significantly lower pliance and perhaps in the pathogenesis of ab-
than in patients with DKA without abdominal pain dominal pain. Patients with DKA and abdominal
(15 Ϯ 1 mmol/L and 7.24 Ϯ 0.09, respectively, both pain had a greater history of alcohol (51%) and co-
P Ͻ .0001). The association between abdominal caine abuse (13%) compared with those without
pain and severity of metabolic acidosis was con- abdominal pain (24% and 2%, respectively, both
firmed by ␹2 analysis of trend (P Յ .0001). The re- P Ͻ .001).
lationship between admission levels of bicarbonate, In all patients without an identifiable cause of
glucose, and osmolality and the presence of ab- abdominal pain, the pain spontaneously resolved
dominal pain is shown in Table 2. Pain was present after resolution of metabolic acidosis. In such pa-
tients, the mean duration of insulin therapy until
resolution of ketoacidosis was 12 Ϯ 2 hours. Two
Table 2. Admission Serum Bicarbonate, Glucose, patients died during the study period, 1 patient with
and Osmolality Levels in Patients With DKA DKA admitted with Fournier’s necrotizing fasciitis,
and Abdominal Pain and 1 patient in the HHS group who was admitted
No. Patients with urosepsis and bladder malignancy.
Total No. (%) With
DKA Patients Abdominal Pain
DISCUSSION
Bicarbonate (mmol/L)
Ͻ5 29 25 (86) The evaluation of abdominal pain in patients
5 to Ͻ10 47 31 (66) with DKA may be difficult and frequently chal-
10 to Ͻ15 66 24 (36) lenges the physicians’ clinical acumen. Faced with
15-18 47 26 (13) a seriously ill patient, the clinician must judge
Glucose (mg/dL)
whether the abdominal pain is a consequence of the
Ͻ400 55 20 (36)
400-600 60 29 (48) metabolic decompensation or if the pain signals a
Ͼ600 74 37 (50) serious underlying intra-abdominal process that
Calculated osmolality (mmol/kg) may have precipitated the development of ketoaci-
Ͻ300 63 30 (48) dosis. Because of the fear of missing an intra-
300-320 89 36 (40)
abdominal medical or surgical process, extensive
Ͼ320 37 20 (54)
laboratory and radiologic studies may be ordered.
NOTE. Total serum osmolality was calculated as follows:
However, in the majority of such patients, the ab-
[2 ϫ sodium ion (mEq/L)] ϩ [glucose (mg/dL)/18] ϩ [blood
urea nitrogen (mg/dL)/2.8], with normal values being 290 Ϯ 5
dominal pain is likely to resolve with correction
mmol/kg of water. To convert glucose values to mmol/L, of ketoacidosis. In some instances, exploratory la-
divide glucose (mg/dL) by 18. parotomy is performed without positive results,

66 UMPIERREZ AND FREIRE

increasing the cost of medical care, and the shown to impair gastrointestinal motility in dia-
morbidity and mortality risk in patients with betic patients and in normal subjects.17-21 Although
DKA.12-14 Until now, the prevalence and clinical delayed gastric emptying may be related to neuro-
significance of gastrointestinal symptoms, includ- pathic changes,19-21 acute hyperglycemia has been
ing abdominal pain in patients with HHS, have not shown to produce gastroparesis by a direct effect.21
been prospectively evaluated. Similarly, acute hyperglycemia has adverse ef-
Abdominal manifestations including nausea, fects on esophageal motility and gallbladder con-
vomiting, and abdominal pain are frequently re- tractility.22-24 It is also possible that increased cir-
ported in patients with DKA. In agreement with culating levels of glucagon and catecholamines
previous reports,7,8,12,16 the cause of the abdomi- in DKA may delay gastrointestinal motility.7 In
nal pain in most patients could not be identified by addition, the abdominal pain in DKA has been
clinical and radiologic studies, but the pain spon- attributed to rapid expansion of the hepatic cap-
taneously resolved after resolution of ketoacidosis. sule, presumably secondary to fatty liver,7,8 or
In one third of patients with DKA, the abdominal to bowel ischemia secondary to severe volume
pain was considered to be secondary to the pre- depletion and metabolic acidosis9 or mesenteric
cipitating cause of metabolic decompensation; insufficiency.25,26
however, surgical intervention was required in only In agreement with recent publications,2,27,28 our
5 of 86 (6%) patients with DKA and abdominal study indicates that omission of insulin and poor
pain. compliance with medical therapy is a major pre-
Our study indicates that the abdominal pain in cipitating cause of DKA in urban patients. Several
DKA is associated with a more severe metabolic studies have indicated that patients with diabetes
acidosis compared with those without abdominal and substance abuse are twice as likely to fail to
pain. Based on the recent classification of severity take their insulin in the 24 hours before hospital-
of DKA,1 75% of the patients with severe DKA ization.27-29 In addition to its role in decreased com-
presented with pain, but only 13% with mild DKA pliance, a history of alcohol and cocaine abuse may
experienced abdominal pain. In contrast, we ob- play a role in the pathogenesis of abdominal pain
served no association between the presence of ab- and metabolic decompensation. Alcohol excess
dominal pain and the initial blood glucose level may be complicated with alcoholic pancreatitis and
and/or severity of dehydration. The admission blood ketoacidosis,30 and cocaine may precipitate mesen-
glucose and serum osmolality were similar between teric ischemia.31,32 In addition, animal and human
DKA patients with and without abdominal pain. studies,33-35 have shown that cocaine increases the
Moreover, none of the patients with HHS presented concentration of counterregulatory hormones, in-
with abdominal pain despite the fact that they were cluding epinephrine, norepinephrine, corticotropin,
admitted with a mean blood glucose concentration and cortisol, which might act as a precipitating fac-
greater than 1,000 mg/dL and a mean serum osmo- tor for DKA.
lality greater than 350 mOsm/L. Although the num- In summary, our study indicates that gastroin-
ber of patients with HHS in this study is too small testinal manifestations including nausea, vomiting,
to reach a definitive conclusion on the lack of asso- and abdominal pain are common in patients with
ciation between abdominal pain and HHS, our re- DKA. The presence of abdominal pain was asso-
sults indicate that in patients with mild DKA or in ciated with a more severe metabolic acidosis and
the absence of significant metabolic acidosis, it may with a history of alcohol or cocaine abuse, but not
be dangerous to attribute abdominal pain to the with the severity of hyperglycemia or dehydration.
metabolic decompensation. Although a potential acute abdominal problem
The pathogenesis of reversible gastrointestinal prompting surgical intervention should not be over-
symptoms in patients with DKA has not been rig- looked, in the majority of patients, the abdominal
orously defined, and may be multifactorial, in- pain spontaneously resolves after correction of the
volving metabolic, humoral, and neural processes. metabolic disturbance. In the absence of an overt
Nausea and vomiting have been attributed to either cause for abdominal pain, allowing several hours
a central neurogenic response to increased ketone to treat the underlying acidosis constitutes the best
bodies and acidosis or to gastric atony and gen- diagnostic tool to elucidate the cause of abdominal
eralized ileus.7 Acute hyperglycemia has been pain in ketoacidosis.

ABDOMINAL PAIN IN DKA 67

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