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Ketogenic Diet as Treatment for SeizuresA Case StudyIntroduction:GH was a child admitted to the Primary Children’s Medical Center (PCMC) for four-day consistent fever and a purple macular rash on her face and upper extremities on August 25, 2011. While in the emergency department (ED) she experienced a tonic clonic seizure. She was then admitted to the pediatric intensive care unit (PICU) for treatment. Several days previous to this, she was seen at urgent care and tested positive for E. coli and was started on antibiotics. She reported symptoms of a fever, decreased oral intake, and mild upper respiratory infection (URI) including a stuffy nose, sore throat, swollen lymph gland on the left neck. Her mother called her primary medical doctor (PMD) and was instructed to go to the ED on 8/23. She was seen, treated, and sent home with the belief that she had a viral component to her illness. Her mother stated she appeared to be improving until 8/25 when she awoke early in the AM confused and lethargic. Upon this time she was brought to the ED at PCMC. This case study will discuss her past social and medical history and her treatment and progress at PCMC as well as an overview of the use of the ketogenic diet (KD) for treatment of seizures.Social History:GH is a 9-year 2-month old Caucasian female residing with her father, mother, and younger sister in the Syracuse, Utah. She recently started 4th grade and reportedly enjoys and does well in school. Medical History:GH has a history of urinary reflux that was resolved by age 2. She has had no urinary tract infections since. Other than this, GH is a previously healthy child. Family history is significant for diabetes mellitus and heart disease. Maternal grandmother recently diagnosed with uterine cancer.The Ketogenic Diet as Treatment for SeizuresThe ketogenic diet (KD) is used as a form of treatment for seizures (1). An individual participating in a KD is forced to produce ketones to provide energy for the body, specifically acetoacetate and beta-hydroxybutyrate (BHB) for the brain (2). Originally, fasting was used as a way to force individuals to undergo ketosis but the KD has provided a way to obtain nutrition while still receiving the metabolic effects of fasting (2). The mechanism in which the KD produces an anticonvulsant effect is not completely understood, but it is believed that the ketone bodies produced by individuals undergoing treatment inhibit neurotransmissions that cause seizure episodes (1). Upon initiation of the diet, strict adherence must be kept in order for it to remain effective as a treatment for seizures (2).The KD consists of high fat, moderate protein and low carbohydrates (2). Often it was begun with fasting, but it has been found that fasting is not a necessary process in the initiation of KD (2). Typically individuals would participate in a 24 to 72 hour fast, or until ketone levels of 4+ were present in the urine (1). It has been found that there is no positive outcome with fasting to initiate the KD treatment, as seizure reduction at three months was similar for those who initiated the KD with a fast and those who did not (2). Individuals who did not participate in the typical fast, have fewer negative side effects of hypoglycemia and emesis, which ultimately results in decreased length of hospital stay (2). When designing a KD treatment plan, there are several routes available to take. There are two widely used types of KD plans, traditional and medium chain triglyceride (MCT) (2). Developed in the 1920s, the traditional, or classic, KD approach includes a 4:1 ratio for fat to non-fat calories (1). For children, fat is typically given at 75% of total daily intake (1). The main sources of fat in a KD include vegetable oil, butter, and heavy cream (2). The non fat calories include both protein and carbohydrate, with protein provided at a higher percentage than carbohydrates in order to maintain ketosis as well as provide needed amino acids for growth (1). Protein is typically provided around the range of 1 g/kg/day (1). Low-carbohydrate fruits and vegetables are allowed, while sugar, breads, pastas, grains, and high-carbohydrate fruits and vegetables are not allowed on the classic KD (2). Also, a fluid restriction of 2 L/day is used to prevent dilution of the ketone levels (1). To ensure adequate nutrition, multi-vitamin/mineral and extra calcium supplements are included in the treatment plan (1).The MCT-based KD is the second available approach to the treatment of seizures with ketosis (1). MCT were first used due to their increased palatability over the traditional diet, as MCT oil is odorless, colorless, and tasteless (1). MCTs are also a preferred source of fat due to more easily achieved ketosis than with the long-chain triglycerides used in the traditional diet, resulting in a ratio of fat to nonfat calories of 1:1 (1,2). In the MCT diet, 70% of calories come from fats (2). 50% of the fat calories are MCT and the remaining 20% consist of polyunsaturated fatty acids (2). This allows for more fruits and vegetables, and even small amounts of breads and other starches to be consumed on this diet (1). Fluid restrictions are not warranted in the MCT KD plan (1).Two newer versions of the KD treatment have emerged, the low-glycemic-index treatment and the modified Atkins diet (2). The low-glycemic-index treatment plan consists of a diet with two main guidelines to be followed: 60% of calories from fat and an elimination of foods with a glycemic index rating greater than 50 (2). Protein is provided at the rate of 1 g/kg/day (2). The modified Atkins treatment plan consists of a diet of 65% of calories from fat and limited carbohydrates (2). Both of the newer variations of the KD have no published studies to assure their efficacy, however short term use has shown positive outcomes (2). Adherence to a KD may be difficult for some individuals, especially adolescents and teenagers, due to decreased palatability and complexity of meal planning (1,2). As such, a ratio of 2:1 or 1:1 fat to protein and carbohydrate may be used initially (2). Starting KD treatment earlier in life results in better compliance (2). This makes it advisable to initiate the KD as early as possible with individuals suffering from seizures (2). Participating in KD treatment is not only complex due to the limitation on foods individuals are able to consume, but also because individuals and their caregivers must learn to read labels and weigh their foods to ensure the adequate ratio of fat to nonfat grams (2). Adherence to the KD treatment may be negatively affected by the side effects (2). Constipation is the most commonly reported side affect of KD (2). Other undesirable side effects include: diarrhea, abdominal pain, gastroesophageal reflux disease, nephrolithiasis, growth retardation and abnormal laboratory values(1,2). As the individual is unable to consume a well balanced diet, nutritional side effects such as hypoproteinemia and micronutrient deficiencies occur (2). More complex problems that can be caused by following a KD include pancreatitis, hemolytic anemia, and Fanconi renal tubular acidosis (2). These negative side affects must be weighed against the positive outcomes of seizure reduction to determine if the KD is an effective treatment for each individual (1).In a study of infants with a mean age of 1.2, both length and weight were lower than normal after six months of participating in the KD treatment (3). Over the six month period normal length and weight growth for age was 6.1 cm and 1.5 kg respectively, with infants on the KD only gaining 5.1 cm and 1.4 kg (3). A long-term survey consisting of questionnaires completed by individuals or caregivers has shown a limited catch-up growth (4). Although the majority of individuals who had participated in KD treatment were smaller in stature and weight, their complete metabolic panel laboratory values were generally found to be normalized upon cessation of the diet (4). Abnormal lipid levels were also found to normalize with time even for those still actively following the KD (4).Although there are various unpleasant side effects of following a KD, the positive effect of decreased seizures may likely outweigh the negative (1). Decreased events may be seen as quickly as one to three months of initiating the diet (2). The study of infants showed a greater than 50% improvement in spasms for 64% of study participants after 6 months, which increased to 77% improvement after 1-2 years (3). After a median of 2.4 months, 37% of infants were seizure-free for a period of six months (3). Developmental improvements were found in 67% of infants and electroencephalogram (EEG) improvement was found in 32% of infants (3). Thirty percent of study participants were able to decrease the number of anticonvulsants while on KD (3). Also important to note, is the greater than 90% improvement in spasms for infants starting the KD treatment who had tried fewer anticonvulsant medications and were older at onset of spasms (3). As reported by caregivers and individuals in the long-term survey, 80% experienced fewer seizures than before starting the KD (4). Although most individuals and caregivers would not use the KD as a first-line treatment, they would use it after no more than two other treatment options had unsuccessfully been tried (4). The diet is discontinued immediately if episodes worsen or the adverse effects are not handled well by the individual (2). If no progress has been made with seizures after three and a half months on the KD, a rapid discontinuation is recommended (2). If KD is effective as a treatment for seizures, the diet is tapered to a more normalized after two years (1). The fat to nonfat ratio is gradually decreased, allowing more carbohydrates and protein in the diet until ketosis no longer occurs (2). Anthropometrics:GH was 142.2 cm (91%ile) and weighed 28.8 kg (46%ile) upon admit. Her BMI was calculated to be 14.3, which is at the 11%ile for age. Her IBW was36 kg, with an IBW of 80%. No previous weights were available as this was her first hospitalization. Mother reported no concerns with growth prior to hospitalization. Medications:GH was currently receiving several medications while at PCMC. She was receiving vitamin D, calcium and carnitine dietary supplements. Her vitamin D supplementation was in the form of calciferol and her calcium supplementation was in the form of calcium carbonate. She also received carnitor to increase her carnitine levels, as her levels were being depleted by Depakote, an antiepileptic medication. She was receiving Pentobarbital and Versed to keep her sedated. Norcuron was given pro re nata (prn) to assist in muscle relaxation for her endotracheal intubation as well as another paralyzing agent. She was receiving methylpredisone and cellcept to assist in autoimmune and inflammation control. She was receiving several medications to assist in preventing epileptic episodes including: Topamax, Lacosamide, Keppra, Depakote, Vimpat, and Felbatol. The ketogenic diet (KD) was also initiated as treatment for epilepsy. Chlorhexidine was used as an antibacterial oral rinse and Triamcinolone Acetonide was used to treat tongue ulcers. Potassium citrate was being administered as a urinary alkilizer. She was also receiving several maintanence medications including Prevacid for gastrointestinal (GI) ulcer prophylaxis and Lacrilube as an ocular lubricant. PRN she was receiving intravenous (IV) fluids of NaCl 0.9%, Tylenol, Motrin, Zantac, Benadryl and Miralax. Laboratory Data:The following tables contain laboratory data pertinent to current diagnosis:DateKetones, Urine (mg/dl)NormalNegative, Desired level while on Ketogenic Diet is 4+9/29Negative9/281+ H9/271+ H9/26Negative9/25Negative9/24Negative9/23Trace H9/22Trace H9/21Trace H9/20Trace H9/19Trace H9/182+ H9/173+ H9/163+ H9/152+ H9/143+ H9/121+ H9/111+ H9/101+ H9/9NegativeThe ketones are present in the diet due to ketogenic diet administration, and are therefore desirable. The desired level of 4+ was never reached upon the duration of the ketogenic diet treatment. DateWhole Blood GlucoseNormal60-115 mg/dL9/27169 H9/19819/18177 H9/17119 H9/15949/14799/13939/131039/13759/12959/12899/12999/12989/11939/11849/10779/10859/9909/9919/3158 H9/3152 H9/2126 H9/1155 H9/1132 H9/1121 H High blood glucose levels likely associated with stress as GH was in critical condition. Steroid administration also likely contributed to elevated blood glucose levels. DateValproic Acid (ug/dl)Normal50-1259/2858.99/2773.89/2655.49/2557.59/2467.99/2363.99/2271.49.2167.49/2060.69/1950.69/18529/1711 L9/1338.1 L9/1233.5 L9/1127.6 LThe valproic acid test is used to assess adequacy of the anticonvulsant medications she was receiving. Low levels indicate inadequate administration of the medication. Levels increased to normal range upon increased dosage of medication. Comprehensive Metabolic PanelDateNaKClCO2Anion GapGlucBUNCreatCaProAlbBili, totalALPALTASTNormal137-146 mmol/L3.4-4.7 mmol/L98-109 mmol/L17-25 mmol/L3-16 mmol/L60-115 mg/dL7-18 mg/dL0.23-0.61 mg/dL8.8-10.1 mg/dL6.2-8.1 g/dL3.4-5.3 g/dL0.2-1.3 mg/dL175-420 U/L10-35 U/L15-40 U/L9/281453.610428 H13121 H70.3 17.5 L7.12.5 L0.2108 L20399/261433.810627 H1083110.377.4 L7.22.3 L0.1 L98 L1847 H9/241413.89930 H12106100.378.4 L6.1 L3.0 L0.1 L120 L21339/221375.3 H100231493120.48.873.3 L0.3113 L12359/201424110 H2111106130.358.5 L6.43.0 L0.293 L27369/16128 L3.985 L30 H131153 L0.238.3 L6.63.0 L0.3103 L3256 H9/131383.510223137690.387.9 L6.72.9 L0.3116 L1862 H9/91394.410228 H9100170.58 L6.22.7 L0.2103 L19388/291372.8 L10525710005 L0.427.1 L4.3 L2.0 L<0.1 L78 L3368 H8/2513841072291036 L0.407.6 L5.1 L2.7 L<0.1 L111 L3361 HThe abnormal electrolyte levels are likely iatrogenic and were never a big problem with GH. Bicarbonate (CO2) was elevated possibly due to respiratory depression as well as seizures producing lactic acid. Glucose (Gluc) was normal throughout most of hospitalization, but did go high occasionally. Elevated blood glucose can likely be attributed to stress and steroid administration. Blood urea nitrogen (BUN) was low upon admit, likely due to poor per os (PO) prior to admit. Serum calcium (Ca) low due to low albumin, as Ca binds to albumin (alb) in the blood. Low albumin and protein (pro) likely due to low PO intake prior to admit. Albumin stayed low throughout hospital stay, likely due to decreased production as it is a negative acute phase protein. As C-reactive protein (CRP) was consistently elevated, albumin was consistently low. Bilirubin (bili) likely fell below normal ranges due to pentobarbital medication, which causes low bilirubin levels. Alkaline phosphatase (ALP) levels were consistently low, which can be a sign of low zinc status however zinc was checked and level was found to be normal. It is especially interesting for her ALP to be low because many anti-epileptic medications may cause higher ALP levels. Low ALP due to unknown etiology. Aspartate transaminase (AST) was high likely due to the seizures GH was plete Blood Count DateWBCRBCHGBHctMCVMCHMCHCRDWPLTSMPVNucleated RBCsNormal4.5-13.5 K/uL4-5.2 M/uL11.5-15.5 g/Dl35-45%77-95 fL25-33 pg32-36 g/dL11.3-15.6%150-400 K/uL6.6-10.1 fL/100 WBCs9/287.52.68 L8.3 L27 L100.7 H3130.7 L22.4 H3278.70.39/1818.3 H2.97 L8.8 L27 L90.929.632.619.9 H3709.209/573.02 L8.6 L26.5 L87.728.532.513.9497 H9.20White blood cell (WBC) high likely due to stress and infection in the hospital. Consistently low red blood cell (RBC) levels partially due to blood draws, but mostly due to immunosupressed state of GH due to medications received. Hemoglobin (HGB) and hematocrit (Hct) likely low due to the low levels of RBC’s. Mean cell volume (MCV) can be increased with use of anticonvulsant drugs, as is likely the case with GH. Mean cell hemoglobin concentration (MCHC) decreased upon last testing due to decreased HGB, which is due to decreased levels of RBC. Red blood cell distribution width (RDW) high likely due to low levels of circulating RBC’s. Platelets (PLTS) high upon first week of hospitalization but normalized upon duration of admit. This laboratory value was likely reactive thrombocytosis, possibly elevated due to infection and inflammation. DateCRPZincCarnitine, TotalVitamin D, 25 HydroxyNormal<0.8 mg/dL60-120 ug/dL31-78 umol/L30-80 ng/mL9/91.9 H1036435Zinc, carnitine, and vitamin D, 25 hydroxy were all found to be in the normal range when tested. The CRP was elevated at the time, which can affect the readings of the zinc levels, but as CRP was below 6 mg/dL, the zinc is truly normal. DateCalcium, IonizedNormal1.22-1.48 mmol/L9/281.14 L9/261.2 L9/251.229/241.18 L9/221.21 L9/201.259/181.15 L9/31.38/311.19 L8/281.25Ionized calcium (iCa) is low throughout periods of GH’s hospitalization. This could indicate acute inflammation of the pancreas. This could also be iatrogenic, due to inadequate calcium. DateCRPPrealbuminNormal<0.8 mg/dL12-42 mg/dL9/280.69/261.6 H9/2346 H9/201.5 H389/12349/115.9 H9/91.9 H50 H9/30.8 H8/281.9 H8/251.6 HCRP likely elevated due to high stress of GH due to critical condition. High prealbumin may be associated with prednisone administration to GH.DateTriglyceridesCholesterolNormal35-110 mg/dL107-199 mg/dL9/9209 H1938/29908/28127 HTriglycerides and Cholesterol are typically checked previous to starting a ketogenic diet. GH’s cholesterol was normal, while her triglyceride levels were elevated. They could likely be high due to high blood glucose levels for several days prior to testing. DatePotassiumMagnesiumPhosphorusNormal3.4-4.7 mmol/L1.6-2.3 mg/dL3.7-5.6 mg/dL9/282.19/224.22.19/202.13.5 L9/183.82.9 H9/174.9 H9/144.59/133.6 H9/92.25.09/42.33.1 L9/22.5 H3.79/12.34.38/293.3 L1.72.9 LElevated magnesium levels are likely due to respiratory depression caused by induced sedation. Phosphorus levels likely iatrogenic, due to inadequate intake as no reported diuretics were used prior to low lab values. Potassium levels were slightly low upon first of hospitalization, but normalized and stayed wnl. As such, there is little concern for initial decreased potassium level.Treatment and Progress:On 8/26 GH was admitted to PICU where she was tested to determine etiology of seizures. She was diagnosed with encephalopathy and refractory status epilepticus. An electroencephalogram (EEG) was set up and testing and close observation of GH continued for several days in order to determine etiology of seizures. She was NPO until 8/27 when a NJ tube was placed and Nutren Jr @ 50 ml/hr was ordered. The following day (8/28) GH was sedated with pentobarbol to suppress epileptic bursts and placed on a mechanical vent. NJ feeds were increased. Over the next few days, NJ feeds were monitored for tolerance. Seizures continued and anticonvulsant medications were administered throughout hospitalization. Etiology of seizures remained unknown despite extensive testing. On 9/1 Pedialyte @20 ml/hr was added to dietary order. This was a mistake as it was not recommended by dietary staff and the nurse practitioner notice and had it discontinued. Constipation became an issue for GH, with medications started to assist in bowel motility. GH also became hyperglycemic due to steroid therapy, but insulin was not required for treatment. GH became at risk for decreased GI motility secondary to narcotics and pentobarb. Fleets enema was given, miralax administration was increased to bis in die (BID) and glycerin suppository was started once a day. Stool output was reported within normal limits (wnl). Proton pump inhibitors (PPI) were added for additional GI protection while on steroid therapy. On 9/9 GH appeared euvolemic on current diet and fluid intake and was started on ketogenic diet (KD). The KD was started at a 4:1 ratio of fat to nonfat calories, using 149 grams of ketocal powder mixed with water administered at a rate of 70 ml/hr. Phosphorus, calcium, and Vitamin D supplements were provided in addition to the KD dietary order. Laboratory values were checked as protocol. GH tolerated initation of the KD with stable BG but without ketosis at this point. Glucose and ketones were checked every four hours per protocol, with instructions for glucose levels less than 50 being treated with 1 ounce of apple juice. Blood glucose never went below 50 so no corrective action was necessary. The KD treatment was monitored by taking frequent laboratory tests to determine effectiveness and safety of KD. On 9/14 the NJ tube was replaced after pt had emesis and plain frontal supine radiograph of the abdomen (often referred to as a KUB for kidneys, ureter, bladder) demonstrated the NJ was not deep enough. This was the first day a ketone level of 3+ was found in the urine, indicating higher levels of ketosis occurring in the body. On 9/16 GH was diagnosed with respiratory failure related to seizure management (sedation, pentobarbital coma). On 9/17 magnesium was infused to keep serum levels greater than 3 to help with seizure management. Propofol was also started at 150 mcg/kg/min in her IV. On 9/18 GH was diagnosed with hypertension (HTN) and propofol was weaned and was off by 9/19. Electrolytes were managed throughout course of stay with supplements as hypokalemia did occur on 9/20. On 9/22 HTN was no longer issue with GH, and inability to maintain ketosis was discussed and per dietary the reason was believed to be related to steroid use and pentobarb coma. A UTI developed and on 9/23 GH was given antibiotics as treatment. A clot formed in GH’s right arm around the PICC line on 9/24, so lovenox was started and a left PICC line was placed. On 9/29 the plan was to continue the ketogenic diet at least through the weekend and reassess the following week about possible discontinuation of the diet if desired ketosis not achieved. Clinical Evaluation:GH was sedated upon time of assessment. She was on a mechanical vent for assistance in breathing. She was experiencing ulceration in the middle, left side of her tongue. Her skin showed no signs of breakdown. She had experienced muscle wasting due to decreased activity and believed gluconeogenesis occurring. She currently had a foley, and a left brachial PICC DL and PIV in left arm. No clinical seizure activity was noted at time of assessment.Dietary:GH’s acute dietary needs were calculated using PCMCs standard formulations. Her estimated nutrition needs were 1200 kcals (42 kcal/kg), 43-58 g pro (1.5-2.1 g/kg), and 1676 ml fluid (58 ml/kg). Calculations were based on her actual body weight (ABW) of 28.8 kg. GH received increased protein per kg, per critical illness standard values. Calories were increased as well, due to her critical state. Fluid was calculated based on standard equation and was not increased.DateDiet orderPO %Assess tolerance to dietIs diet adequate to meet patient’s needs?9/9/11 13:19Continuous NJ Feed: Ketocal @ 50 ml/hr with free water at additional 20 ml/hrN/APoor – Ketones not at desired 4+ levelNo, Inadequate supply of proteins, carbohydrate, and micronutrients provided.9/1/11Continuous NJ Feed: Nutren Jr @ 50 ml/hr with free water at additional 20 ml/hr plus Pedialyte @ 20 ml/hrN/AGoodYes, Pedialyte added without dietary orders and was subsequently discontinued.8/27/11Continuous NJ Feed: Nutren Jr @ 50 ml/hr with free water at additional 20 ml/hrN/AGoodYes8/25/11NPON/AN/ANoNutrition Screening:Upon day of assessment, GH was at high nutrition risk, according to PCMC’s nutrition screening. Nutrition screening total points were 9 points, with the breakdown as follows: Admit Dx (Seizures) 0 pts; BMI (5-14.9%ile) 1 pt; Diet order (Enteral/TF) 2 pts; Respiratory Status (Mechanical Ventilation) 6 pts. Nutrition Note:Nutrition Assessment(s) and Follow-Up Note(s) based on PCMC format:Assessment: 9/29: Pt still intubated/sedated in pentobarbol coma, on Ketogenic Diet. iCa and phos both low at last test, will assess adequacy of diet/supplementation with Ketogenic Diet RD and discuss need for increased supplementation. Although prealbumin is high, albumin is low and trending?down?and BUN?is normal, but?trending down which can be markers of inadequate protein intake.? Ketones tested negative in urine today (9/28), with previous two days having +1 ketones in urine.? With limited ketone production, ketogenic diet may be ineffective as treatment for seizures.??7 day ave intake (9/22-9/28)?equals 100% of est nutrtitional needs for calories and fluid. Only receiving 1.24 g pro/kg, which is approx 70% of est protein needs. ?9/22: Pt remains in PICU with status epilepticus. Currently on ketogenic diet (4.5:1) and in a pentobarbitol induced coma. No new wt at this time. Nutrition labs show a normal Zinc, Vit D, Pre Alb and Carnitine panel at this time. Pt currently has 0 ketones?in her urine despite a very high ratio and no carbohydrates in her IV fluids or Rx. Suspect the reasoning is two fold: 1) Pt is on steroids. Steroids?cause gluconeogenesis from?visceral protein?- pt is likely catabolizing her visceral protein stores to make her own glucose and 2) Pt is in a pentobarbital coma. The decreased brain activity limits the amount of glucose/ketones needed for?energy. Per NP, pentobarb coma will likely be lightened today and in the near future, but she will cont on steroids for some time.9/16: GH has started Ketocal and is now at 50 ml/hr with additional 20 ml/hr of water via NJ.? Current ratio is 4.5:1.? Urine ketones?were 2+ and now 3+.? Valproic acid has been started.? Meds are in lowest carb form.? Propofol (sourse of IL) is increasing.? Vitamin D level was wnl and?zinc level was wnl. She is receiving additional vitamin D at 800 IU per day with Calcium carbonate and K-Phos secondary to ketogenic diet.9/9: GH is a nine year old female who is currently intubated, and in a medically-induced coma with no positive affect of anti-seizure medications.??The decision to trial the?ketogenic diet for seizure control has been made.???GH is currently NJ fed with Nutren Jr. to equal 1200 calories per day and ~36 grams of protein per day, and 1680 ml per day with additional fluid of 20 ml per hour. Prealbumin is pending to determine adequacy of current calorie/protein intake.? Secondary to low calories because of acute phase needs and high fat requirement of the ketogenic diet, 100% of protein needs are not met by recommended ketogenic diet?formula.? Prealbumin with CRP and weight will need to be checked?while intubated and on the diet every 3-5 days to assess severity of potential malnutrition.??Once, calories can be increased, there?will be more "room" for protein in her formula.??GH will advance to a 4:1 ratio by Tuesday morning.? Formula will advance in 3 stages to full ratio, 1/3 ratio x 8 hours, then 2/3 ratio x 8 hours, then full ratio for 24 hours.??9/6: ?GH is in a chemically induced coma, orally intubated, receiving NJ feeds at goal rate. Feeds are providing 42 kcal/kg/day and 1.3 gm proteinkg/day. Tolerating feeds. No new weight. Prealbumin would be helpful in assessing adequacy of protein intake.8/30: Pt admitted to PICU with new onset seizures, decreased LOC and encephalitis of unknown etiology. Currently intubated and sedated. Post-pyloric feeding tube was placed and enteral feeds have been initiated.Nutrition Diagnosis: 9/29: Inadequate protein intake related to physiological causes increasing nutrient needs due to prolonged catabolic illness as evidenced by elevated glucose and prevention of ketosis despite ketogenic diet.9/9: Risk for inadequate carbohydrate intake related to induction of the Ketogenic diet as evidenced by anticipated low blood sugar and acetate levels.8/30: Inadequate oral intake related to mech vent as evidenced by inability to independently consume PO food/fluids.Goals: 9/29: Non Ketogenic Diet NJ Feeding Goal:?Compleat Pediatric @ 50 ml/hr plus 20 ml/hr water.? Feeds provide 1200 kcal and 45.6 g protein per day.9/9: Promote seizure control by appropriately administering the Ketogenic diet.?8/30: Adequate intake to promote optimal growth and development for age/condition.Interventions: 9/16: Ergocalciferol 800 IU daily; 1250 mg NJ calcium carbonate q 6 hrs; K-ph 500 mg daily. Ketocal at 50 ml/hr with free water at additional 20 ml/hr to total 70 ml/hr continuous NJ feeds.Recommendations: 9/29: Recommend dc’ing ketogenic diet at this time. Pt is not in ketosis and appears to continue to experience gluconeogensis (breaking down of muscle stores to produce endogenous glucose) b/o stress hormones inherent in critical condition. Increasing ratio of ketogenic diet will likely increase gluconeogenesis and continue to prevent ketosis while pt is in a critical state. Please cont to check ketones/BG levels to determine effectiveness of ketogenic diet. Please check Vitamin E to ensure adequate levels and to r/o hemolytic anemia given hx/of high LDH. Please check ammonia levels to help determine if metabolic protein breakdown is occurring. Will as RN to zero bed and obtain new wt as last wt was taken at admit.9/22: Cont to check ketones/BG over the next 3-4 days as pentobarb coma is lightened. Please check Pre Alb and CRP?now. If Pre Alb is declining/low, please consider dc'ing ketogenic diet until pt is off steroids/not critically ill. (Inactive)9/9: Initiate KD via Ketogenic formula on?Friday, September 9, 2011.??First 1/3 strenth ratio will run for 50 ml per hour x 8 hours.? An additional 20 ml per hour of free water may?be administed to reach maintenance fluid.? Second 2/3 strenth ratio will run for 50 ml per hour x 8 hours.? An additional 20 ml per hour of free water may?be administed to reach maintenance fluid.?Full strength ratio of 4:1 can be run at 50 ml per hour x 24 hours once 1/2 and 2/3 strength formulas have been used.? An additional 20 ml per hour of free water may?be administed to reach maintenance fluid.?Please provide no more than 240 ml at each meal.? Please provide no more than 240 ml at a time, i.e. within a one hour period.? Maintenance fluid is ~1676 mL.? Please minimize additional fluid to help with seizure control while on the ketogenic diet. (Inactive)Daily supplements are to include the following, 2 tablets K-Phos Neutral, 600mg Calcium, 800 IU Vitamin D, 1 packet Cytra-K Crystals, and Carnitine per Paula Peterson. Please provide brand name supplements as above to control carbohydrate content. Check?CRP and prealbumin every 5 days. (Inactive) Change all current meds to be ketogenic diet friendly - minimize use of liquids/syrups unless compounded. (Inactive)?9/6: Check Prealbumin, CRP with next labs. Continue 50 ml/hr Nutren Junior plus 20 ml/hr free water NJ feeds.?(Inactive)8/30: Please decrease feeds to 50ml/hr to prevent overfeeding. If maintenance fluids are desired, please run free water @ 20ml/hr. (Inactive)Patient Follow-Up:GH’s medical team continued to discuss possible etiology for seizures as well as reason for inability to achieve ketogenesis. A weight was taken on 9/30, of 25.4kg showing weight loss. On 10/1 pancreatitis was found and GH was taken off KetoCal. Her formula was changed to Vivonex TEN at a rate of 55 ml/hr with a decrease in free water to 15 ml/hr in order to keep fluid regimen the same. To account for the weight loss, estimated needs were calculated at 1350 kcals/day. On 10/4 GH’s NJ tube was replaced past the ligament of Tritez and NJ feeds were continued. At this point in time, the goal is to determine etiology and stop occurrence of GH’s seizures. Until this happens prognosis is poor for GH as she has received long-term sedation with the inability to safely wean, as well as the ineffectiveness of several anticonvulsant medications and the attempted ketogenic diet.References:Remig, Valentina. Medical Nutrition Therapy for Neurologic Disorders. In: Mahan LK, Escott-Stump S, ed. Krause’s Food & Nutrition Therapy. 12 ed. St. Louise, MO: Saunders Elsevier; 2008:1088-1090.Zupec-Kania BA, Spellman E. An Overview of the Ketogenic Diet for Pediatric Epilepsy. Nutr Clin Pract. 2008;23:589-596.Hong AM, Turner Z, Hamdy RF, Kossoff EH. Infantile spasms treated with the ketogenic diet: Prospective single-center experience in 104 consecutive infants. Epilepsia. 2010;51(8):1403-1407.Patel A, Pyzik PL, Turner Z, Rubenstein JE, Kossoff EH. Longer term outcomes of children treated with the ketogenic diet in the past. Epilepsia. 2010;51(7):1277-1282. ................
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