J Pediatr Endocr Met 2014; 27(11-12): 1227–1231
Patient report Wenjing Li, Chunxiu Gong*, Di Wu and Min Liu
Two case reports of severe pediatric hyperosmolar hyperglycemia and diabetic ketoacidosis accompanied with rhabdomyolysis and acute renal failure Introduction
Abstract Objective: This report describes two adolescent males in China who suffered from type 2 diabetes mellitus (T2DM) and hyperglycemic hyperosmolar syndrome (HHS) complicated by rhabdomyolysis (RM). After sufficient fluid administration, both patients recovered. Design: Case report. Results: These two obese patients suffered from T2DM, DKA and HHS. Because of insufficient fluid administration, these patients became aggravated and suffered from RM. After aggressive fluid resuscitation and insulin injection, the conditions of the two patients improved. Insulin administration was ceased after approximately 1 month of subcutaneous injections. The two patients attained good glucose control with diet management. Conclusions: HHS is one of the most severe complications of T2DM. RM is a sign that the condition of a patient with HHS may worsen. Although management strategies are undefined, effective fluid infusion was shown to be helpful. Thus, the early signs of HHS and RM should be recognized so as to avoid severe complications. Keywords: diabetic ketoacidosis (DKA); hyperglycemic hyperosmolar state (HHS); obese adolescent; rhabdomyolysis (RM); type 2 diabetes. DOI 10.1515/jpem-2014-0131 Received March 23, 2014; accepted June 10, 2014; previously published online July 18, 2014 *Corresponding author: Chunxiu Gong, MD, PhD, Endocrinology and Genetics Metabolism Department, Beijing Children’s Hospital, Capital Medical University, No. 56, South Lishi Road, Xicheng District, Beijing, P. R. China, Phone: +86 13370115001, Fax: +86 01059618682, E-mail: [email protected] Wenjing Li, Di Wu and Min Liu: Endocrinology and Genetics Metabolism Department, Beijing Children’s Hospital, Capital Medical University, Beijing, China
Recent trends indicate a rising incidence of type 2 diabetes mellitus (T2DM) in children younger than 18 years, with increases in morbidity due to obesity year after year (1–5). The prevalence of T2DM in patients under the age of 20 in 2050 may be up to four times that in 2010 (6). There are some severe complications of T2DM occurring in adolescents that were previously seen only in adults (7). In addition, the incidence of severe complications has increased in recent years. Hyperglycemic hyperosmolar syndrome (HHS) has been a rare pediatric complication of diabetes mellitus (DM) in the past. HHS is characterized by hyperglycemia and hyperosmolality with or without metabolic acidosis (8, 9). HHS is typically associated with T2DM, while diabetic ketoacidosis (DKA) is usually caused by type 1 DM (10). The prognosis of HHS is worse than that of DKA. HHS might cause thrombosis, rhabdomyolysis (RM), renal failure, and irreversible cardiac arrhythmias (11–13). The medical literature contains a few reports of RM caused by HHS occurring in adolescents with T2DM (7, 14–21). Herein, we report on two adolescent patients newly diagnosed with T2DM complicated with DKA and HHS, and presenting with RM during treatment on the first day after admission. The relevant literature is reviewed, and the experiences of identifying and treating such patients are summarized so as to aid in finding a useful therapeutic regimen.
Case reports The two patients were obese adolescent males, both healthy previously. They were presented at the emergency room and admitted immediately. Case 1 was 11.5 years old and had complained of chest distress for 6 days. He went to another hospital 6 days before admission, where myocarditis was suspected; he
Brought to you by | University of California - San Francisco Authenticated Download Date | 2/17/15 10:16 AM
1228 Li et al.: HHS and DKA with rhabdomyolysis was given glucose solution or nutrients intravenously daily, and he gradually became remarkably lethargic. He had generalized weakness for 2 days, presented polyuria and polydipsia for 10 h, and then was presented to the emergency room. The blood glucose level was high, and urine glucose and ketones were both positive. The patient presented with chest distress and lethargy after being treated with a large infusion of glucose solution. He was diagnosed with T2DM complicated with severe dehydration and DKA based on signs of polydipsia, polyuria, obesity, acanthosis nigricans, and dehydration. The serum glucose level was > 33.3 mmol/L, and the osmolality was > 320 mOsm/L. Urine ketones were positive, and the venous pH was 3 125/50 25.4 +
Case 2 14.5 1 Lethargic + Severe + > 3 135/80 26 +
Table 2 Physical examination and laboratory test data of the two patients. Item
Case 1
Case 2
Blood glucose, mmol/L pH d-3-Hydroxybutyric acid, mmol/L HbA1c,% Sodium, mmol/L Corrected serum sodium, mmol/L Effective serum osmolality, mOsm/L Creatine kinase, IU/L Myoglobin, ng/L Blood urea nitrogen, mmol/L
47.25 6.8 9.47 11.2 134.3 149.2 327.6 20,784 > 1000 17.31
68.11 7.05 11.61 13.0 127 149.3 334.4 12,362 > 1000 12.73
Electromyography was performed; neither myogenic nor neurogenic impairments were found. RM may have been the cause of the myalgia. The patient took regular subcutaneous insulin injections for 33 days. He was discharged and given dietary treatment. Case 2 complained of fatigue for 3 days and polyuria for 1 day. He imbibed a large amount of sugary beverages and milk due to extreme thirst the night before admission, and then he experienced lethargy and stupor. He was sent to our hospital, and it was found that his peripheral blood glucose level was higher than the limit that could be tested; urine ketones and electrolytes were abnormal, etc. He became extremely lethargic after drinking large quantities of cola, fruit juice, and milk. He was diagnosed with T2DM complicated with severe dehydration, DKA, and HHS based on clinical manifestations. Early stage shock was diagnosed due to symptoms of unconsciousness, tachycardia, and the presence of striae on the flanks. Fluid resuscitation was administered immediately. However, after fluid infusion for 13 h, the patient deteriorated to a coma accompanied with a decreased blood pressure and anuria. The urine color after fluid infusion was dark red, and laboratory evaluation revealed elevated creatinine, CK-MB, and myoglobin levels. The diagnosis of RM and acute renal failure was made based on these laboratory tests (Table 1). The fluid infusion speed at the beginning was 11.7 mL/(kg h), and then it was reduced to 2.0 mL/(kg h). As a consequence of an apparently insufficient fluid supplementation, the patient’s urine output and blood pressure decreased, which indicated that the shock was worsening. To increase the fluid supplementation, the speed of the fluid infusion was quickly increased to 5.8 mL/(kg h) combined with the administration of vasoactive agents, which increased the urine output and stabilized the blood pressure. Ten hours later, the infusion speed was decreased to 2.3 mL/(kg h) and the
Brought to you by | University of California - San Francisco Authenticated Download Date | 2/17/15 10:16 AM
Li et al.: HHS and DKA with rhabdomyolysis 1229
administration of vasoactive agents was maintained. The boy recovered consciousness 2 days later. He was treated with regular insulin injections for 1 month. The patient was discharged and kept on dietary treatment.
Discussion The two patients were diagnosed with T2DM combined with severe dehydration, DKA-HHS, and early stages of shock. These are the first two cases of HHS complicated by RM, hypovolemic shock, and acute renal failure out of more than 1700 diabetic patients hospitalized in our hospital in the last 40 years whom we have treated and managed. No RM has been reported to have occurred in diabetic children or adolescents previously. RM is a syndrome characterized by breakdown of muscle tissue, followed by dispersion of its intracellular components into the circulatory system (22). The released intracellular components include electrolytes, purines, enzymes (e.g., creatine kinase), and myoglobin, which cause impairment of body homeostasis and organ function. In diabetic patients with HHS, energy supplementation is insufficient and metabolic disturbances destroy the structure of the muscle cells (23). Hyponatremia, hypernatremia, hypokalemia, and hypophosphatemia may disrupt the cell membrane homeostasis, mainly by disturbing the Na/K ATPase pump, and result in RM (22). Normally, the muscle function in RM patients recovers with no sequelae in most patients. However, life-long weakness and atrophy may persist (24) if large amounts of myocytes become necrotic or the pathogenic factors are not eliminated. Singhal et al. (25) concluded that serum sodium, serum osmolality, and blood glucose are the major determinants for the occurrence of RM in the diabetic state. Both of the patients imbibed sweet drinks or were administered a solution containing glucose, which led to the aggravation of the hyperglycemia. Increasing levels of osmolality and blood glucose might trigger HHS (25). The low level of insulin also results in lipolysis, thus causing ketosis. In T2DM patients, hyperglycemia increases plasma osmolarity and polyuria, resulting in dehydration. After the first step of intravenous fluid compensation, we reduced the speed of fluid infusion according to DKA guidelines, which aggravated the hypovolemic shock. Consequently, ATP production was reduced, causing the ATP-dependent sodium-potassium pump to not function properly, resulting in RM (26). Four cases of T2DM combined with DKA and HHS, with the development of RM, have been reported in the
literature (20). Successful treatment depended on a large fluid infusion given at an early stage, at a speed of 7–15 mL/(kg h) over 10 h. All patients experienced successful fluid resuscitation at the early stages, but regardless of the intensive treatment, all suffered from RM. One patient was newly diagnosed with T2DM combined with DKA and HHS (7). An insufficient fluid supply caused the RM. Another patient (14) was complicated with slight RM during fluid therapy at an early stage of severe shock. The Pediatric Association of the Netherlands (NVK) guideline distinguishes the treatment of DKA from HHS. Correction of intravascular hypovolemia with fluid replacement is the most important initial treatment in children with HHS. If adequate fluid replacement does not decrease serum glucose levels satisfactorily, administration of insulin should be considered (12). Massive osmotic diuresis in HHS patients can result in severe dehydration, with fluid losses estimated to be twice as those of DKA patients (27). The hypertonicity of the hyperosmolar state maintains the intravascular volume, which can mask the clinical signs of dehydration. Low osmolality in plasma can result in water movement from the intravascular to the intracellular space (11). For both patients described here, the severity of dehydration may have been underestimated due to patient obesity, which caused the inadequate fluid resuscitation. Singhal et al. (25) reported that serum osmolality levels and blood glucose are the major determinants of the occurrence of rhabdomyolysis in the diabetic state. Insufficient fluid infusion might be the main cause of RM. When patients are treated for severe HHS and acidosis, the severe damage due to dehydration must be adequately considered and appropriate management should be carried out under intensive supervision (28). In the cases reported here, the low speed of fluid infusion aggravated the condition of dehydration, which was reversed by increasing the fluid infusion speed. Although the combination of HHS and DKA with T2DM in children has been reported, there is no standard protocol available for management (29, 30). We recommend treating RM caused by HHS with the following methods. To treat dehydration due to HHS, fluid infusion equal to 12–15% of the body weight should be administered (7). Patients with HHS should undergo more rapid fluid replacement than that recommended for DKA patients (31). A minimum initial bolus of 20 mL/kg of isotonic saline (0.9% NaCl) with repeated boluses should be given until peripheral perfusion is restored. After the initial boluses, the fluid deficit should be replaced over 1–2 days (7). Colloid fluid may be administered intravenously if necessary. After volume expansion, vasoactive agents can be administered once needed. For adult patients, it
Brought to you by | University of California - San Francisco Authenticated Download Date | 2/17/15 10:16 AM
1230 Li et al.: HHS and DKA with rhabdomyolysis is recommended (26) that 0.9% saline is initially administered at 1500 mL/h, followed by 300–500 mL/h when the circulatory volume is stable. In addition, the urine output should be > 200 mL/h. The choice of the fluid should be individualized based on serum electrolytes (7). Sever et al. (32) reported that mannitol administration can remove liquids from the damaged muscular interstitium and increase urine output, which might prevent acute kidney failure. However, Cervellin et al. (26) proposed that there is little clinical support for the use of bicarbonate, mannitol, or furosemide. In addition, hemodialysis may be initiated when water and electrolyte disturbances or acute renal failure exists (33). Furthermore, appropriate adequate fluid administration can lower the serum glucose level. Low-dose and late insulin administration is recommended (7, 28). Here, we reported two cases of patients diagnosed with RM caused by DKA-HHS in adolescents with T2DM in China. These cases highlight that severe complications may occur in pediatric diabetic patients. RM has also been reported in a patient suffering from fulminant type 1 DM (34); therefore, early and aggressive fluid resuscitation and intensive monitoring may prevent severe complications such as acute renal failure and reduce the mortality. Funding: The Capital Development Fund 2009-1046.
References 1. Liu LL, Lawrence JM, Davis C, Liese AD, Pettitt DJ, et al. Prevalence of overweight and obesity in youth with diabetes in USA: the SEARCH for Diabetes in Youth study. Pediatr Diabetes 2010;11:4–11. 2. Mayer-Davis EJ, Beyer J, Bell RA, Dabelea D, D’Agostino RJ, et al. Diabetes in African American youth: prevalence, incidence, and clinical characteristics: the SEARCH for Diabetes in Youth Study. Diabetes Care 2009;32:S112–22. 3. Liu LL, Yi JP, Beyer J, Mayer-Davis EJ, Dolan LM, et al. Type 1 and Type 2 diabetes in Asian and Pacific Islander U.S. youth: the SEARCH for Diabetes in Youth Study. Diabetes Care 2009;32:S133–40. 4. Bell RA, Mayer-Davis EJ, Beyer JW, D’Agostino RJ, Lawrence JM, et al. Diabetes in non-Hispanic white youth: prevalence, incidence, and clinical characteristics: the SEARCH for Diabetes in Youth Study. Diabetes Care 2009;32:S102–11. 5. Haines L, Wan KC, Lynn R, Barrett TG, Shield JP. Rising incidence of type 2 diabetes in children in the U.K. Diabetes Care 2007;30:1097–101. 6. Imperatore G, Boyle JP, Thompson TJ, Case D, Dabelea D, et al. Projections of type 1 and type 2 diabetes burden in the U.S. population aged
Patient report Wenjing Li, Chunxiu Gong*, Di Wu and Min Liu
Two case reports of severe pediatric hyperosmolar hyperglycemia and diabetic ketoacidosis accompanied with rhabdomyolysis and acute renal failure Introduction
Abstract Objective: This report describes two adolescent males in China who suffered from type 2 diabetes mellitus (T2DM) and hyperglycemic hyperosmolar syndrome (HHS) complicated by rhabdomyolysis (RM). After sufficient fluid administration, both patients recovered. Design: Case report. Results: These two obese patients suffered from T2DM, DKA and HHS. Because of insufficient fluid administration, these patients became aggravated and suffered from RM. After aggressive fluid resuscitation and insulin injection, the conditions of the two patients improved. Insulin administration was ceased after approximately 1 month of subcutaneous injections. The two patients attained good glucose control with diet management. Conclusions: HHS is one of the most severe complications of T2DM. RM is a sign that the condition of a patient with HHS may worsen. Although management strategies are undefined, effective fluid infusion was shown to be helpful. Thus, the early signs of HHS and RM should be recognized so as to avoid severe complications. Keywords: diabetic ketoacidosis (DKA); hyperglycemic hyperosmolar state (HHS); obese adolescent; rhabdomyolysis (RM); type 2 diabetes. DOI 10.1515/jpem-2014-0131 Received March 23, 2014; accepted June 10, 2014; previously published online July 18, 2014 *Corresponding author: Chunxiu Gong, MD, PhD, Endocrinology and Genetics Metabolism Department, Beijing Children’s Hospital, Capital Medical University, No. 56, South Lishi Road, Xicheng District, Beijing, P. R. China, Phone: +86 13370115001, Fax: +86 01059618682, E-mail: [email protected] Wenjing Li, Di Wu and Min Liu: Endocrinology and Genetics Metabolism Department, Beijing Children’s Hospital, Capital Medical University, Beijing, China
Recent trends indicate a rising incidence of type 2 diabetes mellitus (T2DM) in children younger than 18 years, with increases in morbidity due to obesity year after year (1–5). The prevalence of T2DM in patients under the age of 20 in 2050 may be up to four times that in 2010 (6). There are some severe complications of T2DM occurring in adolescents that were previously seen only in adults (7). In addition, the incidence of severe complications has increased in recent years. Hyperglycemic hyperosmolar syndrome (HHS) has been a rare pediatric complication of diabetes mellitus (DM) in the past. HHS is characterized by hyperglycemia and hyperosmolality with or without metabolic acidosis (8, 9). HHS is typically associated with T2DM, while diabetic ketoacidosis (DKA) is usually caused by type 1 DM (10). The prognosis of HHS is worse than that of DKA. HHS might cause thrombosis, rhabdomyolysis (RM), renal failure, and irreversible cardiac arrhythmias (11–13). The medical literature contains a few reports of RM caused by HHS occurring in adolescents with T2DM (7, 14–21). Herein, we report on two adolescent patients newly diagnosed with T2DM complicated with DKA and HHS, and presenting with RM during treatment on the first day after admission. The relevant literature is reviewed, and the experiences of identifying and treating such patients are summarized so as to aid in finding a useful therapeutic regimen.
Case reports The two patients were obese adolescent males, both healthy previously. They were presented at the emergency room and admitted immediately. Case 1 was 11.5 years old and had complained of chest distress for 6 days. He went to another hospital 6 days before admission, where myocarditis was suspected; he
Brought to you by | University of California - San Francisco Authenticated Download Date | 2/17/15 10:16 AM
1228 Li et al.: HHS and DKA with rhabdomyolysis was given glucose solution or nutrients intravenously daily, and he gradually became remarkably lethargic. He had generalized weakness for 2 days, presented polyuria and polydipsia for 10 h, and then was presented to the emergency room. The blood glucose level was high, and urine glucose and ketones were both positive. The patient presented with chest distress and lethargy after being treated with a large infusion of glucose solution. He was diagnosed with T2DM complicated with severe dehydration and DKA based on signs of polydipsia, polyuria, obesity, acanthosis nigricans, and dehydration. The serum glucose level was > 33.3 mmol/L, and the osmolality was > 320 mOsm/L. Urine ketones were positive, and the venous pH was 3 125/50 25.4 +
Case 2 14.5 1 Lethargic + Severe + > 3 135/80 26 +
Table 2 Physical examination and laboratory test data of the two patients. Item
Case 1
Case 2
Blood glucose, mmol/L pH d-3-Hydroxybutyric acid, mmol/L HbA1c,% Sodium, mmol/L Corrected serum sodium, mmol/L Effective serum osmolality, mOsm/L Creatine kinase, IU/L Myoglobin, ng/L Blood urea nitrogen, mmol/L
47.25 6.8 9.47 11.2 134.3 149.2 327.6 20,784 > 1000 17.31
68.11 7.05 11.61 13.0 127 149.3 334.4 12,362 > 1000 12.73
Electromyography was performed; neither myogenic nor neurogenic impairments were found. RM may have been the cause of the myalgia. The patient took regular subcutaneous insulin injections for 33 days. He was discharged and given dietary treatment. Case 2 complained of fatigue for 3 days and polyuria for 1 day. He imbibed a large amount of sugary beverages and milk due to extreme thirst the night before admission, and then he experienced lethargy and stupor. He was sent to our hospital, and it was found that his peripheral blood glucose level was higher than the limit that could be tested; urine ketones and electrolytes were abnormal, etc. He became extremely lethargic after drinking large quantities of cola, fruit juice, and milk. He was diagnosed with T2DM complicated with severe dehydration, DKA, and HHS based on clinical manifestations. Early stage shock was diagnosed due to symptoms of unconsciousness, tachycardia, and the presence of striae on the flanks. Fluid resuscitation was administered immediately. However, after fluid infusion for 13 h, the patient deteriorated to a coma accompanied with a decreased blood pressure and anuria. The urine color after fluid infusion was dark red, and laboratory evaluation revealed elevated creatinine, CK-MB, and myoglobin levels. The diagnosis of RM and acute renal failure was made based on these laboratory tests (Table 1). The fluid infusion speed at the beginning was 11.7 mL/(kg h), and then it was reduced to 2.0 mL/(kg h). As a consequence of an apparently insufficient fluid supplementation, the patient’s urine output and blood pressure decreased, which indicated that the shock was worsening. To increase the fluid supplementation, the speed of the fluid infusion was quickly increased to 5.8 mL/(kg h) combined with the administration of vasoactive agents, which increased the urine output and stabilized the blood pressure. Ten hours later, the infusion speed was decreased to 2.3 mL/(kg h) and the
Brought to you by | University of California - San Francisco Authenticated Download Date | 2/17/15 10:16 AM
Li et al.: HHS and DKA with rhabdomyolysis 1229
administration of vasoactive agents was maintained. The boy recovered consciousness 2 days later. He was treated with regular insulin injections for 1 month. The patient was discharged and kept on dietary treatment.
Discussion The two patients were diagnosed with T2DM combined with severe dehydration, DKA-HHS, and early stages of shock. These are the first two cases of HHS complicated by RM, hypovolemic shock, and acute renal failure out of more than 1700 diabetic patients hospitalized in our hospital in the last 40 years whom we have treated and managed. No RM has been reported to have occurred in diabetic children or adolescents previously. RM is a syndrome characterized by breakdown of muscle tissue, followed by dispersion of its intracellular components into the circulatory system (22). The released intracellular components include electrolytes, purines, enzymes (e.g., creatine kinase), and myoglobin, which cause impairment of body homeostasis and organ function. In diabetic patients with HHS, energy supplementation is insufficient and metabolic disturbances destroy the structure of the muscle cells (23). Hyponatremia, hypernatremia, hypokalemia, and hypophosphatemia may disrupt the cell membrane homeostasis, mainly by disturbing the Na/K ATPase pump, and result in RM (22). Normally, the muscle function in RM patients recovers with no sequelae in most patients. However, life-long weakness and atrophy may persist (24) if large amounts of myocytes become necrotic or the pathogenic factors are not eliminated. Singhal et al. (25) concluded that serum sodium, serum osmolality, and blood glucose are the major determinants for the occurrence of RM in the diabetic state. Both of the patients imbibed sweet drinks or were administered a solution containing glucose, which led to the aggravation of the hyperglycemia. Increasing levels of osmolality and blood glucose might trigger HHS (25). The low level of insulin also results in lipolysis, thus causing ketosis. In T2DM patients, hyperglycemia increases plasma osmolarity and polyuria, resulting in dehydration. After the first step of intravenous fluid compensation, we reduced the speed of fluid infusion according to DKA guidelines, which aggravated the hypovolemic shock. Consequently, ATP production was reduced, causing the ATP-dependent sodium-potassium pump to not function properly, resulting in RM (26). Four cases of T2DM combined with DKA and HHS, with the development of RM, have been reported in the
literature (20). Successful treatment depended on a large fluid infusion given at an early stage, at a speed of 7–15 mL/(kg h) over 10 h. All patients experienced successful fluid resuscitation at the early stages, but regardless of the intensive treatment, all suffered from RM. One patient was newly diagnosed with T2DM combined with DKA and HHS (7). An insufficient fluid supply caused the RM. Another patient (14) was complicated with slight RM during fluid therapy at an early stage of severe shock. The Pediatric Association of the Netherlands (NVK) guideline distinguishes the treatment of DKA from HHS. Correction of intravascular hypovolemia with fluid replacement is the most important initial treatment in children with HHS. If adequate fluid replacement does not decrease serum glucose levels satisfactorily, administration of insulin should be considered (12). Massive osmotic diuresis in HHS patients can result in severe dehydration, with fluid losses estimated to be twice as those of DKA patients (27). The hypertonicity of the hyperosmolar state maintains the intravascular volume, which can mask the clinical signs of dehydration. Low osmolality in plasma can result in water movement from the intravascular to the intracellular space (11). For both patients described here, the severity of dehydration may have been underestimated due to patient obesity, which caused the inadequate fluid resuscitation. Singhal et al. (25) reported that serum osmolality levels and blood glucose are the major determinants of the occurrence of rhabdomyolysis in the diabetic state. Insufficient fluid infusion might be the main cause of RM. When patients are treated for severe HHS and acidosis, the severe damage due to dehydration must be adequately considered and appropriate management should be carried out under intensive supervision (28). In the cases reported here, the low speed of fluid infusion aggravated the condition of dehydration, which was reversed by increasing the fluid infusion speed. Although the combination of HHS and DKA with T2DM in children has been reported, there is no standard protocol available for management (29, 30). We recommend treating RM caused by HHS with the following methods. To treat dehydration due to HHS, fluid infusion equal to 12–15% of the body weight should be administered (7). Patients with HHS should undergo more rapid fluid replacement than that recommended for DKA patients (31). A minimum initial bolus of 20 mL/kg of isotonic saline (0.9% NaCl) with repeated boluses should be given until peripheral perfusion is restored. After the initial boluses, the fluid deficit should be replaced over 1–2 days (7). Colloid fluid may be administered intravenously if necessary. After volume expansion, vasoactive agents can be administered once needed. For adult patients, it
Brought to you by | University of California - San Francisco Authenticated Download Date | 2/17/15 10:16 AM
1230 Li et al.: HHS and DKA with rhabdomyolysis is recommended (26) that 0.9% saline is initially administered at 1500 mL/h, followed by 300–500 mL/h when the circulatory volume is stable. In addition, the urine output should be > 200 mL/h. The choice of the fluid should be individualized based on serum electrolytes (7). Sever et al. (32) reported that mannitol administration can remove liquids from the damaged muscular interstitium and increase urine output, which might prevent acute kidney failure. However, Cervellin et al. (26) proposed that there is little clinical support for the use of bicarbonate, mannitol, or furosemide. In addition, hemodialysis may be initiated when water and electrolyte disturbances or acute renal failure exists (33). Furthermore, appropriate adequate fluid administration can lower the serum glucose level. Low-dose and late insulin administration is recommended (7, 28). Here, we reported two cases of patients diagnosed with RM caused by DKA-HHS in adolescents with T2DM in China. These cases highlight that severe complications may occur in pediatric diabetic patients. RM has also been reported in a patient suffering from fulminant type 1 DM (34); therefore, early and aggressive fluid resuscitation and intensive monitoring may prevent severe complications such as acute renal failure and reduce the mortality. Funding: The Capital Development Fund 2009-1046.
References 1. Liu LL, Lawrence JM, Davis C, Liese AD, Pettitt DJ, et al. Prevalence of overweight and obesity in youth with diabetes in USA: the SEARCH for Diabetes in Youth study. Pediatr Diabetes 2010;11:4–11. 2. Mayer-Davis EJ, Beyer J, Bell RA, Dabelea D, D’Agostino RJ, et al. Diabetes in African American youth: prevalence, incidence, and clinical characteristics: the SEARCH for Diabetes in Youth Study. Diabetes Care 2009;32:S112–22. 3. Liu LL, Yi JP, Beyer J, Mayer-Davis EJ, Dolan LM, et al. Type 1 and Type 2 diabetes in Asian and Pacific Islander U.S. youth: the SEARCH for Diabetes in Youth Study. Diabetes Care 2009;32:S133–40. 4. Bell RA, Mayer-Davis EJ, Beyer JW, D’Agostino RJ, Lawrence JM, et al. Diabetes in non-Hispanic white youth: prevalence, incidence, and clinical characteristics: the SEARCH for Diabetes in Youth Study. Diabetes Care 2009;32:S102–11. 5. Haines L, Wan KC, Lynn R, Barrett TG, Shield JP. Rising incidence of type 2 diabetes in children in the U.K. Diabetes Care 2007;30:1097–101. 6. Imperatore G, Boyle JP, Thompson TJ, Case D, Dabelea D, et al. Projections of type 1 and type 2 diabetes burden in the U.S. population aged
