妊娠与儿童健康杂志

抽象的

Adjunct Therapy with Ketogenic Diet to Infant Bacterial Meningitis

Jiaying Feng, Jianxiang Liao*, Lili Pan, Dezhi Cao, Tieshua Huang, Jing Duan, Sufang Lin and Aizhen Yu

Background: Bacterial meningitis is still a common disease in China, and has long hospital stay of about one month and high incidence of fatality and sequelae. We assumed that ketogenic diet (KD) could increase the low glucose in the cerebral spinal fluid, provide energy to brain, shorten the hospital stay and decrease the incidence of its fatality and sequelae, because of its action of anti-microorganisms, inflammation, antiseizure and neuroprotection. Method: Reviewing the patient’s charts. This is a retrospective case study of two consecutive early infant cases with bacterial meningitis. Results: After consulted to an infant who was with meningococcal bacterial meningitis and had left severe occipital encephalomalacia, came the infant girl with bacterial meningitis, because of three days fever and a 30 minutes seizure. Blood culture got pneumonia streptococcus and cerebral spinal fluid (CSF) smear gram stain positive bacteria. The glucose was 0.02 mmol/L and cell count was 326*10^6/L in her CSF, even if the blood glucose was 3.8 mmol/L. She was treated with routine treatment: antibiotics and dexamethasone. On day 2, her frequent focal seizures originated from the left side brain because of the magnetic resonance scan demonstrated subdural emission were deterioratedlasted 11 days, PICU stay 2 days. Informed consent was gotten and medical ethnic permission was approved. On day three of admission KD was initiated by fasting for 29 hours, then her blood betahydroxybutyric acid level reached 2.3 mmol/L, and then with 2:1 Qitong (Zeneca, China) liquid ketogenic diet. 3 days later the ratio of KD increased to 3:1. On day 7, three days after ketosis the glucose in cerebral spinial fluid increased quickly from 0.02 mmol/L to 1.98 mmol/L and white cell counts and protein decreased significantly within one week as well. The blood glucose level was 3.94 ± 0.51 mmol/L (n=30), range 2.8-5.3 mmol/L, median 3.9 mmol/L, 95% CI 3.75-4.13 mmol/L. The blood ketone body (beta-hydroxybutyric acid) level was 1.5 ± 0.82 mmol/L (n=21), range 0.5-3, median 1.2 and 95% CI 1.13-1.88 mmol/L. On day 9 and day 10 of admission the blood betahydroxytutyric acid level was 2.28 ± 0.58 (n=8, range and median, 1.4-3.0,2.4) mmol/L, blood glucose level was 4.13 ± 0.32 (n=8, range and median, 3.7-4.8, 4.10). From day 11, frequent monitoring of blood glucose and ketone body was discontinued. 29 days later she was discharged from hospital. The KD was discontinued after 3 months. The blood sugar and ketone bodies was monitored about every 6 h in hospital, then ketone bodies were monitored two times weekly. After 5.5 months the MRI scan showed mild atrophy of the left brain. Follow-up was performed 1, 3, 6, 12 and 24 months. No symptomatic hypoglycemia and other significant complications happened. No more seizures happened. Her physical and neuropsychological development is similar to that of her same age children at last follow-up. Conclusion: KD might be a safe and effective adjunctive therapy for bacterial meningitis, increasing the glucose in cerebral spinal fluid quickly and inhibiting the inflammation process. It might reduce the complications and sequalae of bacterial meningitis. Further investigations including clinical trial with more cases need to be performed.