Differentiating Hypoglycemia from other diseases

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Differentiating Hypoglycemia from other Diseases

Neonatal hypoglycemia should be differentiated from other causes of neurological symtpoms in neonates:

Disease
Sepsis
Inborn errors of metabolism
Hyponatremia
perinatal asphyxia

In neonates, nonspecific signs of sepsis are often similar to those of hypoglycemia, such as irritability, lethargy, and tachypnea.

Because of the serious consequences,

empiric antibiotic therapy should be provided (after cultures are obtained) to infants with suspected sepsis pending definitive culture-based diagnosis, in addition to administrating interventions directed towards hypoglycemia.

Metabolic diseases that often present between 12 and 72 hours of age after the initiation of oral feeding include hyperglycinemia, urea cycle disorders, and branched-chain organic acidemias. Hypoglycemia may also be an associated finding in patients with some metabolic diseases (table 1) and will persist despite measures to increase blood glucose levels. The diagnosis of inborn errors of metabolism and specific disorders is discussed separately.

Patients typically are not symptomatic until serum or plasma sodium falls below 125 mEq/L, and present with neurologic manifestations including lethargy, obtundation, and, eventually, seizures. The diagnosis of hyponatremia is made by obtaining serum electrolyte levels

Neonatal encephalopathy can present with lethargy and irritability, but symptoms fail to improve with an increase in blood glucose levels. Evidence by magnetic resonance imaging of acute brain injury confirms the diagnosis of encephalopathy. 

Diseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings
Na+, K+, Ca2+ CT /MRI CSF Findings Gold standard test Neck stiffness Motor or Sensory deficit Papilledema Bulging fontanelle Cranial nerves Headache Fever Altered mental status
Brain tumour[1][2] Cancer cells[3] MRI Cachexia, gradual progression of symptoms
Delirium tremens Clinical diagnosis Alcohol intake, sudden witdrawl or reduction in consumption Tachycardia, diaphoresis, hypertension, tremors, mydriasis, positional nystagmus,
Subarachnoid hemorrhage[4] Xanthochromia[5] CT scan without contrast[6][7] Trauma/fall Confusion, dizziness, nausea, vomiting
Stroke Normal CT scan without contrast TIAs, hypertension, diabetes mellitus Speech difficulty, gait abnormality
Neurosyphilis[8][9] Leukocytes and protein CSF VDRL-specifc

CSF FTA-Ab -sensitive[10]

Unprotected sexual intercourse, STIs Blindness, confusion, depression,

Abnormal gait

Viral encephalitis Increased RBCS or xanthochromia, mononuclear lymphocytosis, high protein content, normal glucose Clinical assesment Tick bite/mosquito bite/ viral prodome for several days Extreme lethargy, rash hepatosplenomegaly, lymphadenopathy, behavioural changes
Herpes simplex encephalitis Clinical assesment History of hypertension Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy Normal History of alcohal abuse Ophthalmoplegia, confusion
CNS abscess leukocytes >100,000/ul, glucose and protien, red blood cells, lactic acid >500mg Contrast enhanced MRI is more sensitive and specific,

Histopathological examination of brain tissue

History of drug abuse, endocarditis, immune status High grade fever, fatigue,nausea, vomiting
Drug toxicity Lithium, Sedatives, phenytoin, carbamazepine
Conversion disorder Diagnosis of exclusion Tremors, blindness, difficulty swallowing
Electrolyte disturbance or Depends on the cause Confusion, seizures
Febrile convulsion Not performed in first simple febrile seizures Clinical diagnosis and EEG Family history of febrile seizures, viral illness or gastroenteritis Age > 1 month,
Subdural empyema Clinical assesment and MRI History of relapses and remissions Blurry vision, urinary incontinence, fatigue
Hypoglycemia ↓ or Serum blood glucose

HbA1c

History of diabetes Palpitations, sweating, dizziness, low serum, glucose

References

  1. Soffer D (1976) Brain tumors simulating purulent meningitis. Eur Neurol 14 (3):192-7. PMID: 1278192
  2. Weston CL, Glantz MJ, Connor JR (2011). "Detection of cancer cells in the cerebrospinal fluid: current methods and future directions". Fluids Barriers CNS. 8 (1): 14. doi:10.1186/2045-8118-8-14. PMC 3059292. PMID 21371327.
  3. Yeh ST, Lee WJ, Lin HJ, Chen CY, Te AL, Lin HJ (2003) Nonaneurysmal subarachnoid hemorrhage secondary to tuberculous meningitis: report of two cases. J Emerg Med 25 (3):265-70. PMID: 14585453
  4. Lee MC, Heaney LM, Jacobson RL, Klassen AC (1975). "Cerebrospinal fluid in cerebral hemorrhage and infarction". Stroke. 6 (6): 638–41. PMID 1198628.
  5. Birenbaum D, Bancroft LW, Felsberg GJ (2011). "Imaging in acute stroke". West J Emerg Med. 12 (1): 67–76. PMC 3088377. PMID 21694755.
  6. DeLaPaz RL, Wippold FJ, Cornelius RS, Amin-Hanjani S, Angtuaco EJ, Broderick DF; et al. (2011). "ACR Appropriateness Criteria® on cerebrovascular disease". J Am Coll Radiol. 8 (8): 532–8. doi:10.1016/j.jacr.2011.05.010. PMID 21807345.
  7. Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG; et al. (2012). "Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients". J Neurol Sci. 317 (1–2): 35–9. doi:10.1016/j.jns.2012.03.003. PMID 22482824.
  8. Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  9. Ho EL, Marra CM (2012). "Treponemal tests for neurosyphilis--less accurate than what we thought?". Sex Transm Dis. 39 (4): 298–9. doi:10.1097/OLQ.0b013e31824ee574. PMC 3746559. PMID 22421697.


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