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CASE REPORT
Year : 2014  |  Volume : 17  |  Issue : 5  |  Page : 658-661

Hyperglycemic crisis precipitated by Lassa fever in a patient with previously undiagnosed type 2 diabetes mellitus


Department of Medicine, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State, Nigeria

Date of Acceptance27-Dec-2014
Date of Web Publication22-Sep-2014

Correspondence Address:
A E Edo
Department of Medicine, University of Benin Teaching Hospital, PMB 1111, Benin City, Edo State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1119-3077.141445

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   Abstract 

Hyperglycemic crisis (HC) is an acute complication of diabetes mellitus (DM) that is commonly precipitated by infections and non-compliance with therapy. Viral precipitant of HC is uncommon. To report a rare case of HC unmasked by Lassa fever in a patient previously not known to have diabetes mellitus. A 54 year old lady presented with complaints of generalized body weakness, inability to pass stool, and fever. There was no abdominal pain, vomiting and nausea. There were no features of DM. She is not a known case of diabetes mellitus or hypertension. Patient does not drink alcoholic beverages. There was no history of bleeding from any orifices. She was acutely ill-looking, afebrile, not pale, anicteric, nil pedal oedema. Pulse rate was 110 beats per minute, regular, normal volume. Blood pressure was 110/80 mmHg. Respiratory rate was 26 cycles/minute, breath sound was vesicular. Abdomen was full and moved with respiration. There were no areas of tenderness, no organomegaly, no ascites, and bowel sounds were normoactive. Neurologic examination revealed a conscious patient who was restless. Casual blood glucose was 600mg/dl. Urinalysis: Glycosuria (+++), HbA1c was 12.4%. Lassa PCR done was positive. Patient was managed for hyperglycemic crisis with intravenous normal saline and soluble insulin. She was also commenced on Ribavirin but died of complications of lassa fever. Lassa fever should be included as a precipitant of hyperglycemic crisis in endemic countries.

Keywords: Hyperosmolar hyperglycemic state, lassa fever, precipitating factor


How to cite this article:
Edo A E, Okaka E, Ezeani I U. Hyperglycemic crisis precipitated by Lassa fever in a patient with previously undiagnosed type 2 diabetes mellitus. Niger J Clin Pract 2014;17:658-61

How to cite this URL:
Edo A E, Okaka E, Ezeani I U. Hyperglycemic crisis precipitated by Lassa fever in a patient with previously undiagnosed type 2 diabetes mellitus. Niger J Clin Pract [serial online] 2014 [cited 2022 Jan 24];17:658-61. Available from: https://www.njcponline.com/text.asp?2014/17/5/658/141445


   Introduction Top


Hyperglycemic crisis (HC) is an acute complication of diabetes mellitus (DM) that is potentially life-threatening if left untreated. HC is commonly precipitated by infections (UTI, pneumonia), malaria, intercurrent illness (i.e., surgery, trauma, myocardial infarction, and pancreatitis), psychological stress, non-compliance to insulin therapy, and unidentifiable causes. [1] Viral precipitants are not commonly reported. H1N1 influenza has been reported to be the precipitant in a case of new-onset ketosis-prone diabetes in a 31-year-old Chinese woman with H1N1-influenza. [2] Diabetic ketoacidosis (DKA) has been precipitated by genital herpes infection. [3] Three patients developed DM within 2-3 weeks of acute Hepatitis a virus (HAV) infection associated with DKA. [4] We report a case of hyperglycemic crisis precipitated by Lassa fever in a patient not previously known to have diabetes mellitus.


   Case Report Top


A 54-year-old female pastor was admitted via Accident and Emergency Department on the 2/1/2012, with complaints of generalized body weakness of one week duration, inability to pass stool of six days duration, and fever of one day duration. There was no yellowness of the eyes. Fever was low-grade and continuous. There was no abdominal pain, abdominal distension, nor vomiting and nausea. There were no features of DM. She was not a known case of diabetes mellitus or hypertension. There was no family history of diabetes mellitus. Patient did not smoke cigarette or drink alcoholic beverages. There was no history of bleeding from any orifice.

Physical examination

She was acutely ill-looking, afebrile, not pale, anicteric, and had no pedal edema. Pulse rate was 110 beats per minute, regular, normal volume. Blood pressure was 110/80 mmHg. Apex beat was in the fifth left intercostal space, lateral to the mid-clavicular line. Respiratory rate was 26 cycles/minute, breath sound was vesicular. Abdomen was full and moved with respiration. There were no areas of tenderness, no organomegaly, no ascites, and bowel sounds were normoactive. Neurologic examination revealed a conscious patient who was restless. There were no cranial nerve deficits. Neck was supple. Glasgow Coma Scale score was 15/15. Pupils were equal and reactive to light. Muscle tone, power, and reflexes were normal globally. The clinical diagnosis was mixed hyperglycemic state precipitated by presumed sepsis in a newly diagnosed type 2 diabetes mellitus patient.

Results of investigations

PCV 40%, RBS 600 mg/dl, glycosylated hemoglobin (HbA 1 c) was 12.4%, blood film for malaria parasite was negative. Retroviral screening, HBsAg, and HCV were all negative. Repeat malaria parasite (3/1/12): Trophozites of malaria parasite seen (+).

Urine microscopy: RBCs 5-6 cells, Pus cells 3-4 cells, Cast: Nil, Crystals: Uric acid.

Urine culture yielded no growth after 48 hours s of incubation.

Urinalysis: Glycosuria (+++), Ketonuria (+), calculated plasma osmolality was 341.9 mOsmol/Kg.

WBC 18,000/μl, Granulocytes 13.4 × 10 3 /μl,

Hb 10.5 g/dl, PCV 30%, Platelet 124,000/μl,

Repeat WBC 22,700/μl,

Neutrophils 91%, Lymphocytes 6%, Eosinophils, Monocytes, and Basophils were 3%, ESR 6 mm/hr.

PT 14 secs (control 13 secs); PTTK 44 secs (control 45 secs). Crude clotting time: 22 mins.

Peripheral blood film report showed the following:

Erythrocyte: Anisopoikilocytosis, some nucleated red cells, fragmented cells, tear drops, target cells

Granulocyte: Increased left shift with toxic granulation

Lymphocyte: Adequate in number, normal morphology

Platelet: Adequate in number, some giant forms seen

Conclusion of blood film report was that of stressed marrow with evidence of sepsis.

Other results are summarized in [Table 1] and [Table 2].
Table 1: Laboratory results


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Table 2: Hematologic results

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Cranial CT scan and chest x-ray were requested for but were not done due to the withdrawal of medical services by medical staff of the hospital. The pH of blood and serum lactate is not routinely done in our hospital.

Management

She was admitted into the female medical ward and was commenced on treatment for HC using the usual protocol: Rehydration was carried out with intravenous infusion of 0.9% normal saline. One liter of 0.9% normal saline was given fast, 1 L of 0.9% normal saline was given over the next 30 min, 1 L of 0.9% normal saline was given over the next 1 h, 1 L of 0.9% normal saline was given over the next 2 h, and 500 mL of infusion was given every 4 h. The infusion was changed to 5% dextrose in saline when casual blood glucose dropped to <250 mg/dL. Soluble insulin was then added to 5% dextrose infusion. Hyperglycemia was controlled by giving bolus intravenous soluble insulin 10 units stat and intramuscular soluble insulin 10 units stat, then iv soluble insulin 6-8 units every hour until casual blood glucose ≤250 mg/dL. Soluble insulin was then added to 5% dextrose infusion. Good glycemic control was subsequently achieved.

Subcutaneous enoxaparin 40 mg daily, intravenous ciprofloxacin 200 mg every 12 hours, and intravenous metronidazole 500 mg every 8 hours were also given.

New development while on admission

Medical services were shut down in the hospital due to industrial action (strike) by medical staff of the hospital. She was transferred to the Intensive Care Unit of the hospital on social ground for further management and close monitoring.

She developed marked suprapubic and renal angle tenderness after a day on admission and by the third day of admission, the urine output reduced (input/output = 1750 mL/800 mL) and blood pressure rose to 180/110 mmHg. Patient was commenced on Amlodipine 5 mg daily and Lisinopril 5 mg daily. On the fourth day of admission, blood pressure dropped to 90/50 mmHg. The anti-hypertensives were discontinued. Her clinical condition remained poor. There was worsening dyspnea. She had coarse crepitations in right lower zone. Patient was connected to the mechanical ventilator via the breathing circuit and was placed on SIMV mode. PCV was 19%. There was no evidence of bleeding or blood loss. Lassa PCR done was positive.

Treatment with iv Ribavirin 33 mg/kg stat then 16 mg/kg hrly from day 1-4, thereafter 8 mg/kg 8 hrly day 5-10 was commenced. Other treatments included iv Dexamethasome 6 mg 6 hrly for 48-72 hrs, iv Ceftazidine 1 g 8 hrly. She was transfused with fresh whole blood 1 pint daily for 3 days.

Patient was reviewed by a consultant nephrologist and iv frusemide 140 mg stat with 20 mg/hr by infusion for 6 hrs was added. However, her clinical status continued to deteriorate, and she lapsed into a state of unconsciousness. She was reviewed by a consultant neurologist. Her pupils were fixed and dilated, unreactive to light; oculo-cephalic reflex was absent. An assessment of brain death was made. This was to be confirmed with ambulatory EEG. Unfortunately, patient had a cardiac arrest. Resuscitation efforts were immediately commenced but proved futile, and patient was certified dead after 30 mins of resuscitatory efforts.


   Discussion Top


The common hyperglycemic crises are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Hyperglycemic crisis is a continuum with DKA at one end and HHS at the other end. Some patients have mixed hyperglycemic crisis consisting of features of both DKA and HHS such as metabolic acidosis and hyperosmolarity. [5] Viral precipitants are not commonly reported. Leading precipitating factors of DKA in different countries are similar. Infections were the precipitant of DKA in 30% of cases in Peru [6] and in 30% in India. [7] Infections also ranked among the leading precipitants of hyperglycemic emergencies in Johannesburg, Africans, [8] in Southern Jordan, [9] in Israel, [10] in Brazil, [11] in Kenya, [12] and in Saudi Arabia. [13] Malaria, urinary tract infection, and respiratory infections accounted for 31% of precipitants of DKA in Benin city, Nigeria. [14]

This is the first case to our knowledge of hyperglycemic crisis precipitated by Lassa fever. Because this is an uncommon precipitant, the diagnosis was not initially considered. Lassa fever is a viral hemorrhagic fever. The incubation period of Lassa fever ranges from 7 to 21 days. Majority of cases are asymptomatic. Those that are symptomatic may present with fever and other non-specific symptoms such as general weakness and malaise as found in malaria. Gastrointestinal manifestations such as vomiting and diarrhea are also common. The current knowledge of Lassa fever pathogenesis does not include the chain of events that take place during disease development and leads to death of severely-ill patients. [15]

Patients with Lassa fever develop evidence of vascular damage. Although hemorrhagic manifestations are not important features of Lassa fever, signs of increased vascular permeability such as petechiae, shock, multifocal hemorrhaging, and neurologic signs like coma indicate a poor prognosis. [15] Our patient had features suggestive of sepsis. She later developed multi-organ failure comprising acute renal failure, cardiogenic shock, and coma. The history of fever, restlessness, multi-organ involvement, and a sudden drop in PCV level were the pointer to a possible viral illness in this patient.

There is no established causal link between diabetes mellitus and Lassa fever infection. It would appear that diabetes mellitus was unmasked by Lassa fever in this patient considering the fact that her glycosylated hemoglobin HbA1c was 12.4%. Values of HbA1c of 6.5% and above is suggestive of chronic glycemia of 6-8 weeks. DM is asymptomatic and undiagnosed in up to 25% of the general population. Lassa fever should be considered a possible precipitating factor of hyperglycemic crisis in Lassa fever-endemic areas or countries as early diagnosis and prompt treatment will prevent a fatal outcome in such patients.

Challenges in managing this patient

This patient was managed when medical services were withdrawn by medical staff due to industrial action. Resident doctors and some consultants had to be mobilized to assist in managing this patient who was a doctor's mother. Patient was too weak to be taken out of the ICU to do radiological investigations outside the hospital.

Limitations in diagnostic procedures

There were serious limitations in diagnostic procedures in the management of this patient. These included the inability to do a cranial CT scan for this patient who was initially restless and later lapsed into a state of unconsciousness. Chest X-ray, pH of blood, and serum lactate were also important in the management of this patient but were not done. These limitations resulted largely from paralysis of medical services occasioned by industrial action by medical staff. This case is, however, being reported to bring to the awareness of the medical community that a high index of suspicion is needed in order not to miss the diagnosis of Lassa fever, especially in the setting of hyperglycemic crises.

 
   References Top

1.Umpierrez GE, Kitabchi AE. Diabetic ketoacidosis: Risk factors and management strategies. Treat Endocrinol 2003;2:95-108.  Back to cited text no. 1
    
2.Tan H, Wang C, Yu Y. H1N1 influenza: The trigger of diabetic ketoacidosis in a young woman with ketosis-prone diabetes. Am J Med Sci 2012;343:180-3.  Back to cited text no. 2
    
3.Tesfaye S, Cullen DR, Wilson RM, Woolley PD. Diabetic ketoacidosis precipitated by genital herpes infection. Diabetes Res Clin Pract 1991;13:83-4.  Back to cited text no. 3
    
4.Makeen AM. The association of infective hepatitis type A (HAV) and diabetes mellitus. Trop Geogr Med 1992;44:362-4.  Back to cited text no. 4
    
5.Wachtel TJ, Tetu-Mouradjian LM, Goldman DL, Ellis SE, O'Sullivan PS. Hyperosmolarity and acidosis in diabetes mellitus: A three-year experience in Rhode Island. J Gen Intern Med 1991;6:495-502.  Back to cited text no. 5
    
6.Pinto ME, Villeana JE, Villena AE. Diabetic ketoacidosis in Peruvian patients with type 2 diabetes mellitus. Endocr Pract 2008;14:442-6.  Back to cited text no. 6
    
7.Matoo VK, Nalini K, Dash RJ. Clinical profile and treatment outcome of diabetic ketoacidosis. J Assoc Physicians India 1991;39;379-81.  Back to cited text no. 7
    
8.Zouvanis M, Pieterse AC, Seftel HC, Joffe BI. Clinical characteristics and outcome of hyperglycemic emergencies in Johannesburg Africans. Diabet Med 1997;14:603-6.  Back to cited text no. 8
    
9.Tahboub I, Shalan JB. Diabetic ketoacidosis in southern Jordan: Five-year experience. East Mediterr Health J 2000;6:1035-8.  Back to cited text no. 9
    
10.Barski L, Nevzorov R, Rabaev E, Jotkowitz A, Harman-Boehm I, Zektser M, et al. Diabetic ketoacidosis: Clinical characteristics, precipitating factors and outcomes of care. Isr Med Assoc J 2012;14;299-303.  Back to cited text no. 10
    
11.Weinert LS, Scheffel RS, Severo MD, Cioffi AP, Teló GH, Boschi A, et al. Precipitating factors of diabetic ketoacidosis at a public hospital in a middle-income country. Diabetes Res Clin Pract 2012;96:29-34.  Back to cited text no. 11
    
12.Mbugua PK, Otieno CF, KayimaJK, Amayo AA, McLigeyo SO.Diabetic ketoacidosis: Clinical presentation and precipitating factors at Kenyatta National Hospital, Nairobi. East Afr Med J 2005;82(Suppl 12):S191-6.  Back to cited text no. 12
    
13.Qari FA. Precipitating factors for diabetic ketoacidosis. Saudi Med J 2002;23;173-6.  Back to cited text no. 13
    
14.Edo AE. Clinical profile and outcomes of adult patients with hyperglycemic emergencies managed at a tertiary care hospital in Nigeria. Niger Med J 2012;53:121-5.  Back to cited text no. 14
[PUBMED]  Medknow Journal  
15.Yun NE, Walker DH. Pathogenesis of Lassa fever. Viruses 2012;4:2031-48.  Back to cited text no. 15
    



 
 
    Tables

  [Table 1], [Table 2]


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