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Leukemia presenting as abdominal pain
370
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
m Volume
8, Number
4 m July 1990
3. Bruce RA, Jones JW, Strait GB: Anaerobic metabolic responses to acute maximal exercise in male athletes. Amer Heart J 1964;87:643-850. 4. Hermansen L, Vaage 0: Lactate disappearance and glycogen synthesis in human muscle after maximal exercise.Am J Phvsiol 1977:233(5):E422-E429. 5 Cregler ‘LL: ‘Special report: Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-1500. 6. Giammarco RA: The athlete, cocaine and lactic acidosis: A hypothesis. Am J Med Sci 1987;294(6):412-444.
LEUKEMIA PRESENTING AS ABDOMINAL PAIN* To the Editor: New onset leukemia is a rare cause of acute abdominal pain. Attention to selected signs and symptoms, however, facilitates this diagnosis and avoids unnecessary delays in therapy. The following case underlines the importance of this approach. A 24-year-old Hispanic woman presented to the emergency department (ED) with 12 hours of severe, left upper quadrant (LUQ) abdominal pain. She characterized the pain as sharp and increased with respiration. The patient denied trauma, fever, nausea, vomiting, diarrhea, dysuria, and cough. She did admit to fatigue, malaise, and a 30-pound intentional weight loss over the antecedent 6 months. The patient’s medical history was unremarkable; however, she did have “kidney surgery on the left” as a child. She did not recall the circumstances surrounding this procedure and had no urologic problems since that time. She took no medications and had no allergies . Physical examination revealed an obese female in moderate distress holding the left side of her abdomen. She was alert and vital signs were as follows: oral temperature, 98.2”F; pulse, 105 per minute; blood pressure, 130/84; and respiratory rate, 22 per minute. Chest wall movement was symmetric and the lung fields were clear bilaterally. The cardiac exam was unremarkable. Because of her obesity, abdominal examination was diflicult. Bowel sounds were present and there was left upper quadrant tenderness to deep palpation without rebound or guarding. Neither organomegaly nor costrovertebral angle tenderness were noted. There was a wellhealed scar on the left flank. Rectal examination was normal as was the bimanual pelvic examination. There were no palpable lymph nodes and the remainder of the examination was unremarkable. An acute abdominal radiographic series revealed a soft tissue mass in the left upper quadrant (Fig 1). The white blood cell count was 18O,OOO/~L,hemoglobin 11.9 g/dL, hematocrit 35.9%, and platelet count 189,OOO/~L.There was a preponderance of mature granulocytes on a peripheral blood smear. Pertinent chemistries included a serum sodium of 139 mEq/L, serum potassium of 3.9 mEq/ L, serum creatinine of 0.7 mg/dL, serum phosphorus of 2.5 mgidL, and a serum uric acid of 4.2 mg/dL. The remaining chemistries were normal, as was a routine urinalysis. The patient was admitted with a presumptive diagnosis of granulocytic leukemia. A computed tomographic (CT) scan of the abdomen revealed massive splenomegaly without rupture or hematoma. A bone marrow biopsy was consistent with chronic granulocytic leukemia. The LUQ pain improved with narcotic analgesics. At discharge, the patient was evaluated for bone marrow transplantation. Chronic granulocytic leukemia (CGL) is a disease of unknown etiology typified by leukocytosis and a characteristic differential leukocyte count in the peripheral blood.’ CGL is a variant of the myleoproliferative syndrome which includes myeloid metaplasia, polycythemia Vera, and essential thrombocythemia.* CGL occurs at any age; however, the incidence peaks during middle age and there is a slight male predominance.‘-4 CGL is the least common of the major varieties of leukemia. In western coun*The views expressed in this article are those of the author and do not reflect the official policy of the Department of Defense or other Departments of the US Government.
FIGURE 1.
Supine view of the abdomen shows left upper quadrant mass.
tries, approximately 60% of all leukemias are acute, 25% chronic lymphocytic, and only 15% CGL.‘,4 The etiology of CGL is not known; however, certain risk factors for its development do exist. These include exposure to ionizing radiation, chemical carcinogens (ie, benzene), and certain chemotherapeutic agents.5 There is no evidence supporting viral and genetic etiologies.* Presenting symptoms include malaise, abdominal pain, anorexia, weight loss, and fever.‘-3.6 The sudden onset of sharp LUQ pain may herald splenic rupture or acute splenic enlargement.2*6 Rarely, patients present with acute hemorrhage.‘-3,6 Several nonspecific findings may be identified on physical examination. Anemia is common and a palpable spleen present in 80% of patients. M Splenomegaly can be mild to massive and splenic rupture should be considered in the hypotensive patient with leukemia. Lymphadenopathy is a rare finding. I.6 Certain laboratory findings are unique to CGL. The white blood cell count is usually between 150,000 and 200,000. Hemoglobin and platelet measurements are of no value in making the diagnosis, although the most common picture is one of moderate anemia and thrombocytosis.’ Bone marrow and peripheral smears reveal excessive granulocytes, mostly in the mature form. Other laboratory abnormalities include a low leukocyte alkaline phosphatase (LAP)’ and elevated vitamin B,,.* The most unique laboratory feature of CGL is the presence of the Philadelphia chromosome (Ph’), present in more than 95% of patients with CGL.9 This chromosomal abnormality represents a reciprocal translocation of genetic material between the long arms of chromosomes 22 and 9.9 Based on this hematologic picture, CGL can be divided into two phases, each with particular hematologic findings and prognoses. The first is the chronic phase, which carries a more favorable prognosis. In this instance, the peripheral smears reveal a majority of mature cells. With treatment, the chronic phase lasts from 1 to 5 years. Is3The blast phase represents the ominous transformation from mature granulocytes to blast cells. Frequently, the blast phase is refractory to standard therapy and persists up to 6 months.‘.3 Fatal complications are similar to those found in acute leukemia, namely bleeding and infection.*
CORRESPONDENCE
371
According to Spiers,’ treatment can be divided into urgent, palliative, and curative. The emergency physician may be responsible for initiating urgent therapy. Urgent problems requiring early treatment include severe anemia precipitating angina or congestive heart failure, and hyperuricemia causing renal compromise. Urgent treatment of these problems includes transfusion and the reduction of hyperuricemia with allopurinol. Hyperleukocytosis can lead to deafness, visual impairment, and priapism.’ Leukostasis usually develops at white blood cell counts greater than lOO,OOO/~L,but in CCL these symptoms are uncommon unless the white blood cell count is above 5OO,OOO/pL.’ Hyperleukocytosis is best treated with leukopheresis.’ The ED management of these patients includes hydration and expeditious referral to a hematologist/oncologist. New onset leukemia is uncommon among ED patients. Nevertheless, CCL should be included in the differential diagnosis of leukocytosis and splenomegaly. With proper attention to this blood borne malignancy, substantial morbidity and mortality may be averted. TIMOTHY A. MACLEAN, DO Joint Military Medical Command Emergency Medicine Residency San Antonio, TX
References 1. Spiers A: Chronic granulocytic leukemia. Med Clin North Am 1984;68:713-727 2. Adamson JW: The myleoprolyerative diseases. In Brawnwald E, lsselbacher KT, Petersdorf RG, et al (eds): Harrison’s Principles of Internal Medicine, ed 11. New York, NY, McGrawHill, 1987, pp 1527-1529 3. Rundles RW: Chronic myleogenous leukemia. In Williams WJ, Beutler E, Erslev AJ, et al (eds): Hematology, ed 3. New York, NY, McGraw-Hill, 1983, pp 196-207 4. Gunz FW, Henderson ES: Leukemia. Philadelphia, PA, Grune 8. Stratton, 1983, pp 17-47 5. Bottomlev RH: Etioloav and epidemiology. In Shaw MT (ed): Chronic branulocytic-Leukemia. LondonT-England, Praeger, 1982 8. Spiers AS: The clinical features of chronic granulocytic leukemia. Clin Haematol 1977;6:77-95 7. Wachstein M: Alkaline phosphatase activity in normal and abnormal human blood and bone marrow cells. J Lab Clin Med 1946;31:1-17 8. Beard MF, Pitney RW, Sanneman EH: Serum concentration of vitamin B,* in patients with leukemia. Blood 1954;9:789-794 9. Whang-Peng J, Cancellos GP, Carbone PP, et al: Clinical implication of cytogenic variants in chronic myleogenous leukemia. Blood 1978;32:755-766
WHEN TAC DRIPS INTO THE EYE To the Editor:-We
recently cared for two young children who received 1.5 mL of half-strength TAC (tetracaine 0.25%, adrenaline 1:4,000, cocaine 5.9%) topical anesthetic for the repair of minor facial lacerations located in close proximity to the eye. Each patient
was somewhat noncompliant with the application procedure, and at least one drop of TAC inadvertently came into contact with the ocular surface. Both patients developed anisocoria without other adverse reaction. In each case, fluorescein staining of the cornea did not show an abrasion, and visual acuity was judged to be normal. At follow-up 24 hours later pupils were equally round and reactive to light. Cocaine is a potent topical anesthetic agent that was once used extensively for opthalmologic surgical procedures, until sloughing of the comeal epithelium was commonly noted to occur. TAC contains cocaine, and is most often used to anesthetize dermal lacerations of the face. It is not uncommon for the liquid to inadvertently drip off a cotton or gauze pad applicator; when contacting mucosal surfaces, systemic absorption has resulted in adverse reactions including convulsions, cardiac arrhythmias, and even death. This is the first report of inadvertent TAC instillation into the eye, with anisocoria presumably resulting from cocaine’s ability to block the uptake of catecholamines at adrenergic nerve endings, and potentiate the response of sympathetically-innervated organs to norepinephrine and epinephrine.’ Comeal abrasion or other adverse reaction probably did not develop in either case because a small dose of TAC containing diluted cocaine was utilized. Special care must be exercised when applying TAC to lacerations of the face. Less than 2 mL of half-strength TAC (total dose contains 117 mg cocaine) should be used, which is sufficient to anesthetize 95% of wounds in this area.* When facial wounds are associated with head trauma, routine assessment of pupillary size and reactivity to light should be performed prior to TAC application. With TAC application, the patient should be positioned supine with the head slightly rotated toward the side of the laceration, to ensure that if the medication drips off the applicator it will be directed away from the eyes and mucosal surfaces-caretakers should be instructed to maintain the child in this position throughout the duration of application. Assessment of pupillary size and reactivity to light should be performed prior to discharge. If anisocoria develops, the affected eye should be irrigated to remove any residual medication, and assessment performed for comeal abrasion, with close follow-up to document resolution of abnormalities. WILLIAM A. BONADIO, MD VIRGINIA WAGNER Medical College of Wisconsin Children’s College of Wisconsin Milwaukee, WI
References 1. Ritchie JM, Green NM: Local anesthetics. In Goodman AG, Gilman LS, Gilman A (eds): The Pharmacologic Basis of Therepeutics (ed 17). New York, NY, MacMillan, 1985, pp 302-321 2. Bonadio WA, Wagner V: Half-strength TAC for selected dermal lacerations. Clin Pediatr 1988;27:495-498
ERRATUM
In the article, “Is Emergency Department Resuscitation of Out-of-Hospital Cardiac Arrest Victims Who Arrive Pulseless Worthwhile,” by Lewis et al in the March 1990 issue, the final sentence should have read as follows. “Patients who arrest en route or who have had a transient pulse in the field should not be included in this very poor prognostic group and should be aggressively resuscitated in the ED.”
AMERICAN
JOURNAL
OF EMERGENCY
MEDICINE
m Volume
8, Number
4 m July 1990
3. Bruce RA, Jones JW, Strait GB: Anaerobic metabolic responses to acute maximal exercise in male athletes. Amer Heart J 1964;87:643-850. 4. Hermansen L, Vaage 0: Lactate disappearance and glycogen synthesis in human muscle after maximal exercise.Am J Phvsiol 1977:233(5):E422-E429. 5 Cregler ‘LL: ‘Special report: Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-1500. 6. Giammarco RA: The athlete, cocaine and lactic acidosis: A hypothesis. Am J Med Sci 1987;294(6):412-444.
LEUKEMIA PRESENTING AS ABDOMINAL PAIN* To the Editor: New onset leukemia is a rare cause of acute abdominal pain. Attention to selected signs and symptoms, however, facilitates this diagnosis and avoids unnecessary delays in therapy. The following case underlines the importance of this approach. A 24-year-old Hispanic woman presented to the emergency department (ED) with 12 hours of severe, left upper quadrant (LUQ) abdominal pain. She characterized the pain as sharp and increased with respiration. The patient denied trauma, fever, nausea, vomiting, diarrhea, dysuria, and cough. She did admit to fatigue, malaise, and a 30-pound intentional weight loss over the antecedent 6 months. The patient’s medical history was unremarkable; however, she did have “kidney surgery on the left” as a child. She did not recall the circumstances surrounding this procedure and had no urologic problems since that time. She took no medications and had no allergies . Physical examination revealed an obese female in moderate distress holding the left side of her abdomen. She was alert and vital signs were as follows: oral temperature, 98.2”F; pulse, 105 per minute; blood pressure, 130/84; and respiratory rate, 22 per minute. Chest wall movement was symmetric and the lung fields were clear bilaterally. The cardiac exam was unremarkable. Because of her obesity, abdominal examination was diflicult. Bowel sounds were present and there was left upper quadrant tenderness to deep palpation without rebound or guarding. Neither organomegaly nor costrovertebral angle tenderness were noted. There was a wellhealed scar on the left flank. Rectal examination was normal as was the bimanual pelvic examination. There were no palpable lymph nodes and the remainder of the examination was unremarkable. An acute abdominal radiographic series revealed a soft tissue mass in the left upper quadrant (Fig 1). The white blood cell count was 18O,OOO/~L,hemoglobin 11.9 g/dL, hematocrit 35.9%, and platelet count 189,OOO/~L.There was a preponderance of mature granulocytes on a peripheral blood smear. Pertinent chemistries included a serum sodium of 139 mEq/L, serum potassium of 3.9 mEq/ L, serum creatinine of 0.7 mg/dL, serum phosphorus of 2.5 mgidL, and a serum uric acid of 4.2 mg/dL. The remaining chemistries were normal, as was a routine urinalysis. The patient was admitted with a presumptive diagnosis of granulocytic leukemia. A computed tomographic (CT) scan of the abdomen revealed massive splenomegaly without rupture or hematoma. A bone marrow biopsy was consistent with chronic granulocytic leukemia. The LUQ pain improved with narcotic analgesics. At discharge, the patient was evaluated for bone marrow transplantation. Chronic granulocytic leukemia (CGL) is a disease of unknown etiology typified by leukocytosis and a characteristic differential leukocyte count in the peripheral blood.’ CGL is a variant of the myleoproliferative syndrome which includes myeloid metaplasia, polycythemia Vera, and essential thrombocythemia.* CGL occurs at any age; however, the incidence peaks during middle age and there is a slight male predominance.‘-4 CGL is the least common of the major varieties of leukemia. In western coun*The views expressed in this article are those of the author and do not reflect the official policy of the Department of Defense or other Departments of the US Government.
FIGURE 1.
Supine view of the abdomen shows left upper quadrant mass.
tries, approximately 60% of all leukemias are acute, 25% chronic lymphocytic, and only 15% CGL.‘,4 The etiology of CGL is not known; however, certain risk factors for its development do exist. These include exposure to ionizing radiation, chemical carcinogens (ie, benzene), and certain chemotherapeutic agents.5 There is no evidence supporting viral and genetic etiologies.* Presenting symptoms include malaise, abdominal pain, anorexia, weight loss, and fever.‘-3.6 The sudden onset of sharp LUQ pain may herald splenic rupture or acute splenic enlargement.2*6 Rarely, patients present with acute hemorrhage.‘-3,6 Several nonspecific findings may be identified on physical examination. Anemia is common and a palpable spleen present in 80% of patients. M Splenomegaly can be mild to massive and splenic rupture should be considered in the hypotensive patient with leukemia. Lymphadenopathy is a rare finding. I.6 Certain laboratory findings are unique to CGL. The white blood cell count is usually between 150,000 and 200,000. Hemoglobin and platelet measurements are of no value in making the diagnosis, although the most common picture is one of moderate anemia and thrombocytosis.’ Bone marrow and peripheral smears reveal excessive granulocytes, mostly in the mature form. Other laboratory abnormalities include a low leukocyte alkaline phosphatase (LAP)’ and elevated vitamin B,,.* The most unique laboratory feature of CGL is the presence of the Philadelphia chromosome (Ph’), present in more than 95% of patients with CGL.9 This chromosomal abnormality represents a reciprocal translocation of genetic material between the long arms of chromosomes 22 and 9.9 Based on this hematologic picture, CGL can be divided into two phases, each with particular hematologic findings and prognoses. The first is the chronic phase, which carries a more favorable prognosis. In this instance, the peripheral smears reveal a majority of mature cells. With treatment, the chronic phase lasts from 1 to 5 years. Is3The blast phase represents the ominous transformation from mature granulocytes to blast cells. Frequently, the blast phase is refractory to standard therapy and persists up to 6 months.‘.3 Fatal complications are similar to those found in acute leukemia, namely bleeding and infection.*
CORRESPONDENCE
371
According to Spiers,’ treatment can be divided into urgent, palliative, and curative. The emergency physician may be responsible for initiating urgent therapy. Urgent problems requiring early treatment include severe anemia precipitating angina or congestive heart failure, and hyperuricemia causing renal compromise. Urgent treatment of these problems includes transfusion and the reduction of hyperuricemia with allopurinol. Hyperleukocytosis can lead to deafness, visual impairment, and priapism.’ Leukostasis usually develops at white blood cell counts greater than lOO,OOO/~L,but in CCL these symptoms are uncommon unless the white blood cell count is above 5OO,OOO/pL.’ Hyperleukocytosis is best treated with leukopheresis.’ The ED management of these patients includes hydration and expeditious referral to a hematologist/oncologist. New onset leukemia is uncommon among ED patients. Nevertheless, CCL should be included in the differential diagnosis of leukocytosis and splenomegaly. With proper attention to this blood borne malignancy, substantial morbidity and mortality may be averted. TIMOTHY A. MACLEAN, DO Joint Military Medical Command Emergency Medicine Residency San Antonio, TX
References 1. Spiers A: Chronic granulocytic leukemia. Med Clin North Am 1984;68:713-727 2. Adamson JW: The myleoprolyerative diseases. In Brawnwald E, lsselbacher KT, Petersdorf RG, et al (eds): Harrison’s Principles of Internal Medicine, ed 11. New York, NY, McGrawHill, 1987, pp 1527-1529 3. Rundles RW: Chronic myleogenous leukemia. In Williams WJ, Beutler E, Erslev AJ, et al (eds): Hematology, ed 3. New York, NY, McGraw-Hill, 1983, pp 196-207 4. Gunz FW, Henderson ES: Leukemia. Philadelphia, PA, Grune 8. Stratton, 1983, pp 17-47 5. Bottomlev RH: Etioloav and epidemiology. In Shaw MT (ed): Chronic branulocytic-Leukemia. LondonT-England, Praeger, 1982 8. Spiers AS: The clinical features of chronic granulocytic leukemia. Clin Haematol 1977;6:77-95 7. Wachstein M: Alkaline phosphatase activity in normal and abnormal human blood and bone marrow cells. J Lab Clin Med 1946;31:1-17 8. Beard MF, Pitney RW, Sanneman EH: Serum concentration of vitamin B,* in patients with leukemia. Blood 1954;9:789-794 9. Whang-Peng J, Cancellos GP, Carbone PP, et al: Clinical implication of cytogenic variants in chronic myleogenous leukemia. Blood 1978;32:755-766
WHEN TAC DRIPS INTO THE EYE To the Editor:-We
recently cared for two young children who received 1.5 mL of half-strength TAC (tetracaine 0.25%, adrenaline 1:4,000, cocaine 5.9%) topical anesthetic for the repair of minor facial lacerations located in close proximity to the eye. Each patient
was somewhat noncompliant with the application procedure, and at least one drop of TAC inadvertently came into contact with the ocular surface. Both patients developed anisocoria without other adverse reaction. In each case, fluorescein staining of the cornea did not show an abrasion, and visual acuity was judged to be normal. At follow-up 24 hours later pupils were equally round and reactive to light. Cocaine is a potent topical anesthetic agent that was once used extensively for opthalmologic surgical procedures, until sloughing of the comeal epithelium was commonly noted to occur. TAC contains cocaine, and is most often used to anesthetize dermal lacerations of the face. It is not uncommon for the liquid to inadvertently drip off a cotton or gauze pad applicator; when contacting mucosal surfaces, systemic absorption has resulted in adverse reactions including convulsions, cardiac arrhythmias, and even death. This is the first report of inadvertent TAC instillation into the eye, with anisocoria presumably resulting from cocaine’s ability to block the uptake of catecholamines at adrenergic nerve endings, and potentiate the response of sympathetically-innervated organs to norepinephrine and epinephrine.’ Comeal abrasion or other adverse reaction probably did not develop in either case because a small dose of TAC containing diluted cocaine was utilized. Special care must be exercised when applying TAC to lacerations of the face. Less than 2 mL of half-strength TAC (total dose contains 117 mg cocaine) should be used, which is sufficient to anesthetize 95% of wounds in this area.* When facial wounds are associated with head trauma, routine assessment of pupillary size and reactivity to light should be performed prior to TAC application. With TAC application, the patient should be positioned supine with the head slightly rotated toward the side of the laceration, to ensure that if the medication drips off the applicator it will be directed away from the eyes and mucosal surfaces-caretakers should be instructed to maintain the child in this position throughout the duration of application. Assessment of pupillary size and reactivity to light should be performed prior to discharge. If anisocoria develops, the affected eye should be irrigated to remove any residual medication, and assessment performed for comeal abrasion, with close follow-up to document resolution of abnormalities. WILLIAM A. BONADIO, MD VIRGINIA WAGNER Medical College of Wisconsin Children’s College of Wisconsin Milwaukee, WI
References 1. Ritchie JM, Green NM: Local anesthetics. In Goodman AG, Gilman LS, Gilman A (eds): The Pharmacologic Basis of Therepeutics (ed 17). New York, NY, MacMillan, 1985, pp 302-321 2. Bonadio WA, Wagner V: Half-strength TAC for selected dermal lacerations. Clin Pediatr 1988;27:495-498
ERRATUM
In the article, “Is Emergency Department Resuscitation of Out-of-Hospital Cardiac Arrest Victims Who Arrive Pulseless Worthwhile,” by Lewis et al in the March 1990 issue, the final sentence should have read as follows. “Patients who arrest en route or who have had a transient pulse in the field should not be included in this very poor prognostic group and should be aggressively resuscitated in the ED.”