Easy question of acute complications of diabetes mellitus.

A 76-year-old woman with obesity and type 2 diabetes mellitus on metformin. She comes to the emergency room because for 3 days she presents fever of 38ºC, pollakiuria, dysuria, intense thirst and progressive decrease in her level of consciousness. Physical examination showed signs of dehydration, blood pressure 95/54 mmHg and no signs of neurological focality. The CBC shows leukocytosis, creatinine of 1.8 mg/dL. What is the most likely diagnosis?

Non-ketotic hyperglycemic hyperosmolar hyperglycemic coma.

Renal insufficiency of obstructive cause.

[Severe accidental hypothermia in an elderly woman].

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".

[Diabetic emergencies].

Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.

[Two cases of nonketotic hyperosmolar coma in neurosurgery (author's transl)].

Hyperosmolar nonketotic coma is characterized by hyperglycemia, hyperosmolarity and dehydration in the absence of ketoacidosis. Two cases of hyperosmolar nonketotic coma, in which both the patients recovered, were presented. One of the cases was a 59-year-old female who had suffered from a metastatic brain tumor. After removal of the tumor, the patient's condition improved for a period. This was followed by a period of frequent vomiting, subsequently followed by coma. The laboratory data showed the absence of ketoacidosis in the blood sugar measured at 672 mg/dl and serum osmolarity at 343.1 mOsm./kg. The other case was a 74-year-old female who was admitted to the clinic because of cerebral thrombosis. Her caloric in-take was restricted and insulin was administered because of a mild diabetes mellitus which occured after admission. Then she entered a hyperosmolar non-ketotic coma. The laboratory data revealed blood sugar to be 1068 mg/dl and serum osmolarity to be 418 mOsm./kg. Immediately after large amounts of intravenous drip infusion and insulin were administerd, she recovered from the syndrome. The clinical observations and the pathogenesis of this syndrome were discussed.

[An elderly case of hyperglycemic hyperosmolar non-ketotic coma (HHNC)].

A 79-year old woman was admitted with disturbed consciousness (JCS II-30). She had been given a diagnosis of type 2 diabetes 7 years previously, and was being treated with oral hypoglycemic agents. She also suffered Alzheimer's disease and Parkinson's disease. Plasma glucose and HbA1c upon admission was 676mg/dl and 9.7%, respectively. Serum Na was 153mEq/l. Urine ketone body test was negative and metabolic acidosis was not observed. Hyperglycemic hyperosmolar non-ketotic coma (HHNC) was diagnosed, and treatment was started immediately with normal saline infusion. Continuous infusion of regular insulin was needed to lower blood glucose. Disturbed consciousness and dehydration improved by the third hospital day. However, she became bedridden afterwards and received tube feeding. Up to 46 units of insulin was needed daily to control blood glucose. Urine C-peptide secretion was very low (10microg/day), suggesting that insulin therapy was essential for glycemic control long before admission. It is thought that a number of elderly diabetic patients who need insulin therapy do not receive or continue it for various reasons. Discussion is necessary to grasp the actual situation and defensive actions that can be taken.

[A geriatric case of hyperosmolar hyperglycemic state with osmotic demyelination syndrome that manifested with dysphagia].

The patient was an 84-year-old man who had been on insulin therapy for type 2 diabetes mellitus for 55 years. He had undergone bile duct stenting to avoid obstruction due to adenocarcinoma of the bile duct. The patient had suffered from fever and anorexia for two weeks, and had subsequently stopped insulin therapy. Since he showed signs of impaired consciousness, he was taken to the emergency room, and was diagnosed with a hyperosmotic hyperglycemic state (HHS) based on the following laboratory findings: blood glucose, 632 mg/dL; plasma osmolality, 391 mOsm/kg·H<sub2</subO; and serum Na, 163 mEq/L, with urine ketone bodies±and sepsis (Klebsiella pneumoniae). He was therefore admitted to the hospital. His blood glucose and serum Na levels slowly improved following the administration of fluids, insulin, and antibiotics. The patient's consciousness disturbance also improved. However, on the third day after admission, dysphagia was newly observed when the patient resumed eating, and swallowing endoscopy revealed a delayed gag reflex and pharyngeal retention of saliva. Cranial magnetic resonance imaging showed a high-intensity area in the central pontine, which was considered to be caused by osmotic demyelination syndrome (ODS). The patient's oral intake ability recovered with swallowing rehabilitation. ODS is a rare complication of HHS. We report a case of HHS with ODS, in which the patient's chief complaint was dysphagia, which should be distinguished from other diseases.

Hyperosmolar hyperglycemic state

Signs and symptoms Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyuria), and increased hunger (polyphagia). Symptoms of HHS include: Altered level of consciousness Neurologic signs including: blurred vision, headaches, focal seizures, myoclonic jerking, reversible paralysis Motor abnormalities including flaccidity, depressed reflexes, tremors or fasciculations Hyperviscosity and increased risk of blood clot formation Dehydration Weight loss Nausea, vomiting, and abdominal pain Weakness Low blood pressure with standing Cause The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks.

A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate.

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.

[Non-ketotic hyperosmolar diabetic coma in neurosurgical cases; review of 7 cases].

Neurosurgical patients with non-ketotic hyperosmolar diabetic coma (NHC) in our institution were analysed retrospectively. Seven cases were diagnosed as NHC being 0.47% of the number of inpatients in the last 5 years. The age ranged from 60 to 72 years old (mean 65) and there were 6 males and 1 female. Only 2 patients (29%) had a clear past history of diabetes mellitus. Prior to the NHC, systemic infection was present in 2 cases. Intravenous hyperalimentation (IVH) was performed in 5 cases, glycerol osmotherapy in 3 cases, diphenylhydantion therapy in 3 cases and tube feeding in 2 cases. The overall mortality rate in our series was 71% (5 cases), of which 2 cases died within 2 days due to cardiopulmonary failure, and 3 cases in the chronic stage died due to disseminated intravascular coagulopathy (DIC), or due to renal failure. The prognosis of NHC in neurosurgical patients is generally bad because of the presence of consciousness disturbance prior to the onset of NHC, which may mask the symptoms occurring from the NHC. Other predisposing factors could be systemic infection, IVH or tube feeding, and osmotic agents which are frequently used in neurosurgical patients. There was a tendency for NHC to occur predominantly in the chronic stage after the blood sugar had returned to normal range from the hyperglycemic state in the acute stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyperosmolar hyperglycemic state

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis. Symptoms include signs of dehydration, weakness, leg cramps, vision problems, and an altered level of consciousness. Onset is typically over days to weeks. Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis. The main risk factor is a history of diabetes mellitus type 2. Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1. Triggers include infections, stroke, trauma, certain medications, and heart attacks. Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.

Hyperosmolar hyperglycemic state

Differential diagnosis The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40-50 mmol/L (600 mg/dL). Metabolic acidosis is absent or mild. A temporary state of confusion (delirium) is also more common in HHS than DKA. HHS also tends to affect older people more. DKA may have fruity breath, and rapid and deep breathing. DKA often has serum glucose level greater than 300 mg/dL (HHS is >600 mg/dL). DKA usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics. DKA is characterized by a rapid onset, and HHS occurs gradually over a few days. DKA also is characterized by ketosis due to the breakdown of fat for energy. Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing. Management

Diabetic coma

Nonketotic hyperosmolar coma Nonketotic hyperosmolar coma usually develops more insidiously than diabetic ketoacidosis because the principal symptom is lethargy progressing to obtundation, rather than vomiting and an obvious illness. Extremely high blood sugar levels are accompanied by dehydration due to inadequate fluid intake. Coma occurs most often in patients who have type 2 or steroid diabetes and have an impaired ability to recognize thirst and drink. It is classically a nursing home condition but can occur in all ages. The diagnosis is usually discovered when a chemistry screen performed because of obtundation reveals an extremely high blood sugar level (often above 1800 mg/dl (100 mM)) and dehydration. The treatment consists of insulin and gradual rehydration with intravenous fluids.

Hyperosmolar hyperglycemic state

Diagnosis Criteria According to the American Diabetes Association, diagnostic features include: Plasma glucose level >30 mmol/L (>600 mg/dL) Serum osmolality >320 mOsm/kg Profound dehydration, up to an average of 9L (and therefore substantial thirst (polydipsia)) Serum pH >7.30 Bicarbonate >15 mEq/L Small ketonuria (~+ on dipstick) and absent-to-low ketonemia (<3 mmol/L) Some alteration in consciousness BUN > 30 mg/dL (increased) Creatinine > 1.5 mg/dL (increased) Imaging Cranial imaging is not used for diagnosis of this condition. However, if MRI is performed, it may show cortical restricted diffusion with unusual characteristics of reversible T2 hypointensity in the subcortical white matter.

Diabetic ketoacidosis

If cerebral edema is suspected because of confusion, recurrent vomiting or other symptoms, computed tomography may be performed to assess its severity and to exclude other causes such as stroke. Criteria Diabetic ketoacidosis is distinguished from other diabetic emergencies by the presence of large amounts of ketones in blood and urine, and marked metabolic acidosis. Hyperosmolar hyperglycemic state (HHS, sometimes labeled "hyperosmolar non-ketotic state" or HONK) is much more common in type 2 diabetes and features increased plasma osmolarity (above 320 mosm/kg) due to profound dehydration and concentration of the blood; mild acidosis and ketonemia may occur in this state, but not to the extent observed in DKA. There is a degree of overlap between DKA and HHS, as in DKA the osmolarity may also be increased.

[An elderly case of hyperglycemic hyperosmolar syndrome with hyperketonemia].

A 72-year-old man had been treated for type 2 diabetes mellitus and gastric cancer. He had been receiving insulin and chemotherapy because of diabetes mellitus and terminal gastric cancer. The dose of insulin was decreased due to the appetite loss, but his general condition deteriorated with disturbed consciousness (JCS I-3), so he was admitted to our hospital in November 2006. On admission, he showed abnormal laboratory data such as WBC 11,070/microl, Hb 10.2 g/dl, serum BUN 64.1 mg/dl, serum Cr 2.23 mg/dl, serum CRP 16.78 mg/dl, plasma glucose 830 mg/dl, serum osmolarity 360 mOsm/l, and serum total keton body 5,490 micromol/l. However, serum Na (142 mEq/l), serum K (4.5 mEq/l), arterial blood pH (7.368), and the anion gap (15 mEq/l) were within the normal range. He was given a diagnosis of hyperglycemic hyperosmolar syndrome with hyperketonemia. Immediately treatment was started with physiologic saline and regular insulin infusion. After treatment, glucose level and serum osmolarity ameliorated. Though elderly cases with hyperglycemic hyperosmolar syndrome and hyperketonemia are rarely reported, it is important to be aware that elderly patients often have very atypical signs and symptoms. We report this case to show diverse nature of elderly patients.

Clinical features of hyperosmolar hyperglycemic nonketotic diabetic coma associated with cardiac operations.

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.

Hyperosmolar Hyperglycemic State.

Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose and hyperosmolarity with little or no ketosis. Although there are multiple precipitating causes, underlying infections are the most common. Other causes include certain medications, nonadherence to therapy, undiagnosed diabetes mellitus, substance abuse, and coexisting disease. In children and adolescents, hyperosmolar hyperglycemic state is often present when type 2 diabetes is diagnosed. Physical findings include profound dehydration and neurologic symptoms ranging from lethargy to coma. Treatment begins with intensive monitoring of the patient and laboratory values, especially glucose, sodium, and potassium levels. Vigorous correction of dehydration is critical, requiring an average of 9 L of 0.9% saline over 48 hours in adults. After urine output is established, potassium replacement should begin. Once dehydration is partially corrected, adults should receive an initial bolus of 0.1 units of intravenous insulin per kg of body weight, followed by a continuous infusion of 0.1 units per kg per hour (or a continuous infusion of 0.14 units per kg per hour without an initial bolus) until the blood glucose level decreases below 300 mg per dL. In children and adolescents, dehydration should be corrected at a rate of no more than 3 mOsm per hour to avoid cerebral edema. Identification and treatment of underlying and precipitating causes are necessary.

[Central pontine myelinolysis followed by frequent hyperglycemia and hypoglycemia--report of an autopsy case].

A case of central pontine myelinolysis (CPM) followed by hyperglycemia and hypoglycemia was reported. The case was 53-year-old female. Diabetes mellitus was found when she was 32 years old, insulin therapy was started at 37 years of age. Since she was 50 years old, proteinuria and ankle edema had developed and she was admitted to The Keihin Hospital. The peritoneal dialysis (PD) was performed next year, followed by the hemodialysis (HD). In January 1978, strange movements and the disturbance of her consciousness were occurred during PD, then blood glucose level showed over 1,800 mg/dl and serum osmolarity was over 390 mosm/KgH2O. Then she was diagnosed as non-ketotic hyperosmolar coma. After that, during HD and PD, hyperglycemia (approximately 1,200 mg/dl) and hypoglycemia (approximately 40 mg/dl) developed frequently. She died soon after HD on 19th December 1979. The autopsy disclosed bilateral atrophic kidneys due to diabetic changes and atrophic pancreas. Gross neuropathological findings revealed a few small infarcts at the putamen and the globus pallidus, however, other area were observed to be normal. The most remarkable change in microscopical finding was nearly symmetrical demyelinative lesion in the center of the basis pontis. The nerve cells and axon cylinders were relatively well preserved in the demyelinative lesion. The hyaline degeneration was observed in the arterial wall, however, any arterial obstruction was not found. Recent studies would suggest that the electrolyte disturbance, such as hyponatremia, may lead to CPM, particularly when this disturbance was rapidly corrected. On the other hand, CPM induced by diabetic coma has been reported, however, its pathogenesis has been unclear.(ABSTRACT TRUNCATED AT 250 WORDS)

Dapagliflozin-associated euglycemic diabetic ketoacidosis in a patient with type 2 diabetes mellitus: A case report.

Rare cases of euglycemic diabetic ketoacidosis (eu-DKA) have been reported after the administration of sodium-glucose cotransporter-2 (SGLT-2) inhibitors. No reports have described eu-DKA complicated by hypernatremia due to SGLT-2 inhibitors. A 76-year-old woman with a 40-year history of type 2 diabetes mellitus (DM), for which metformin (1000 mg/day) and dapagliflozin (10 mg/day) were prescribed, presented with malaise, fever, and oliguria. On presentation, her white blood cell count (11,800/μL), serum creatinine (3.2 mg/dL), and C-reactive protein (54 mg/L) were abnormal. Bilateral pyeloureteritis and diffuse paralytic ileus were present. She received intravenous antibiotics and total parenteral nutrition, and was asked to fast. Her renal function and ileus briefly improved. Oral hypoglycemic agents, metformin and dapagliflozin, along with enteral feeding were reinstituted on day 3 of hospitalization. However, on day 6 of hospitalization, the patient developed an altered state of consciousness including confusion, lethargy, and stupor. Several laboratory abnormalities suggestive of ketoacidosis with euglycemia were noted. The patient was diagnosed with eu-DKA accompanied by severe hypernatremia (corrected serum Na concentration, 163 mEq/L) and hypokalemia following dapagliflozin re-administration. The patient was treated with indicated intravenous fluid therapy. Dapagliflozin use was discontinued. The patient's mental status and laboratory findings improved gradually, and she was discharged on maintenance doses of insulin and metformin on day 14 of hospitalization. Acute illnesses such as diffuse paralytic ileus and urinary tract infection, and dietary restrictions or fasting in patients with DM can be considered potential predisposing factors for SGLT-2 inhibitor-associated eu-DKA. For patients with diabetes in the setting of acute morbidity, timely resumption of the SGLT-2 inhibitor therapy should be carefully determined. In addition, eu-DKA due to SGLT-2 inhibitor use may be accompanied by electrolyte disturbances such as hypernatremia and hypokalemia.

Hyperosmolar diabetic non-ketotic coma, hyperkalaemia and an unusual near death experience.

Generally, cardiac arrest due to pulseless electrical activity has a poor outcome, except when reversible factors such as acute hyperkalaemia are identified and managed early. Hyperosmolar diabetic non-ketotic coma may lead to acute hyperkalaemia. Hyperosmolar diabetic non-ketotic coma is a metabolic emergency usually seen in elderly non-insulin dependent diabetics, characterized by severe hyperglycaemia, volume depletion, altered consciousness, confusion and less frequently neurological deficit. Cerebrovascular accident or transient ischaemic attack may be mistakenly diagnosed, particularly if the patient has no history of diabetes mellitus. Delays in diagnosis and management of glycaemic emergencies presenting as a constellation of neurological abnormalities can be avoided by routine early measurement of blood glucose. Hyperosmolar diabetic non-ketotic coma should be considered in any patient with altered consciousness or neurologic deficit in conjunction with hyperglycaemia. As hyperosmolar diabetic non-ketotic coma results in severe fluid depletion, electrolyte disturbance, profound hyperglycaemia and an altered mental state, the guiding principles of therapy include aggressive rehydration, insulin therapy, correction of electrolyte abnormalities and treatment of any underlying illnesses. Treatment of acute hyperkalaemia includes calcium ions, insulin with dextrose, salbutamol and haemodialysis.

Hyperglycemic hyperosmolar non-ketotic syndrome in children with type 2 diabetes*.

Hyperglycemic hyperosmolar non-ketotic (HHNK) syndrome is thought to be a rare entity in the pediatric population, associated with significant mortality based on case reports in the literature. As obesity and type 2 diabetes in childhood grow in prevalence, such related complications may also increase. This study will serve to provide updated information regarding typical clinical course and sequelae of HHNK syndrome in childhood. Patients diagnosed with type 2 diabetes at Children's Hospital of Philadelphia (CHOP) over a period of 5 yr were screened retrospectively for any laboratory evidence of previous episodes of HHNK syndrome. The standard diagnostic criteria of blood glucose >600 mg/dL and serum osmolality >330 mOsm/L with only mild acidosis (serum bicarbonate >15 mmol/L and small ketonuria 15 mg/dL or less) were utilized. The records of all patients with type 2 diabetes mellitus (DM) diagnosed over a 5-yr period were reviewed (n=190). Seven patients were found to have one episode of HHNK syndrome by diagnostic criteria (five males, mean age at presentation 13.3 yr, age range 10.1--16.9 yr), yielding a frequency of 3.7%. All were African-American. HHNK syndrome was the clinical presentation at diagnosis of new onset diabetes for all seven children. Three of seven children had a previously diagnosed developmental delay. The average Glasgow Coma Scale (GCS) score at presentation was 13 (range 9--15). Mean body mass index (BMI) at presentation was 32.7 kg/m(2) (n=6). Mean serum osmolality was 393 mOsm/L (n=7), and mean blood glucose was 1604 mg/dL (n = 7). The average time until mental status returned to baseline among survivors was 3 d (range 1--7 d). The average number of hospital days for survivors was 10 (range 5--24 d). Four of seven patients had an uncomplicated course. One patient developed multisystem organ failure and died on hospital day 4. The case fatality rate was 14.3% (one of seven). Survivors had no appreciable neurodevelopmental sequelae. This retrospective chart review provides updated information regarding the entity of HHNK syndrome in children. This study supports the need for increased awareness of type 2 diabetes in children so that morbidity and mortality related to HHNK syndrome can be prevented.

[Hyperglycemic hyperosmolar nonketotic coma].

Ten patients with the syndrome of non-ketotic hyperosmolar coma are described. The mean age of the patients was 62.3 +/- 17.12 years. One patient was 16 years old. In 9 cases the patients had type II diabetes, one had type I diabetes. In 7 cases the coma was the first sign of diabetes. The factor predisposing in most cases was infection. In the treatment-acting insulin and hypotonic solutions were given. In 2 cases clinical signs of the DIS syndrome were observed manifesting themselves with local changes, including mental disturbances. Heparin was given with good effect. Three patients (30%) died in hospital. The cause of death was serious disease associated with this coma: pancreatitis and myocarditis, purulent bronchopneumonia, myocardial infarction.

Diabetic coma

Diabetic coma is a life-threatening but reversible form of coma found in people with diabetes mellitus. Three different types of diabetic coma are identified: Severe low blood sugar in a diabetic person Diabetic ketoacidosis (usually type 1) advanced enough to result in unconsciousness from a combination of a severely increased blood sugar level, dehydration and shock, and exhaustion Hyperosmolar nonketotic coma (usually type 2) in which an extremely high blood sugar level and dehydration alone are sufficient to cause unconsciousness.

Hypertension Despite Dehydration in an Adolescent with Diabetic Ketoacidosis.

In general, information on blood pressure changes in diabetic ketoacidosis in paediatric population is very scarce. Our aim was to report a case of severe DKA in an adolescent girl who unexpectedly had hypertension rather than hypotension.A 17-year-old girl presented in our Children's Emergency Unit with complaints of excessive eating for 6 weeks, excessive urination for 2 weeks, fever for 1 week, vomiting for 4 days, difficulty with breathing for one day and unresponsiveness to calls for 3 hours. She had moderated to severe dehydration but no hypotension. Laboratory findings included hyperglycaemia (random blood glucose 20.8 mmo/L; 347 mg/dl), acidosis (serum bicarbonate 5 mmol/L),  ketonuria 2+; glycosuria 2+, and urine  specific gravity of 1.015. At admission, the blood pressure was 100/60 mmHg but progressively rose to 140-180/80-100 mmHg by the third day from admission. A significant hypertension can occur in children and adolescents admitted for severe DKA despite the presence of dehydration. Therefore, the attending physician should be aware of this possibility.

Diabetic ketoacidosis

On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, a rapid heart rate and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity" or like "pear drops". The smell is due to the presence of acetone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate. Small children with DKA are relatively prone to brain swelling, also called cerebral edema, which may cause headache, coma, loss of the pupillary light reflex, and can progress to death. It occurs in about 1 out of 100 children with DKA and more rarely occurs in adults.

Hyperosmolar hyperglycemic state.

Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose, hyperosmolarity, and little or no ketosis. With the dramatic increase in the prevalence of type 2 diabetes and the aging population, this condition may be encountered more frequently by family physicians in the future. Although the precipitating causes are numerous, underlying infections are the most common. Other causes include certain medications, non-compliance, undiagnosed diabetes, substance abuse, and coexisting disease. Physical findings of hyperosmolar hyperglycemic state include those associated with profound dehydration and various neurologic symptoms such as coma. The first step of treatment involves careful monitoring of the patient and laboratory values. Vigorous correction of dehydration with the use of normal saline is critical, requiring an average of 9 L in 48 hours. After urine output has been established, potassium replacement should begin. Once fluid replacement has been initiated, insulin should be given as an initial bolus of 0.15 U per kg intravenously, followed by a drip of 0.1 U per kg per hour until the blood glucose level falls to between 250 and 300 mg per dL. Identification and treatment of the underlying and precipitating causes are necessary. It is important to monitor the patient for complications such as vascular occlusions (e.g., mesenteric artery occlusion, myocardial infarction, low-flow syndrome, and disseminated intravascular coagulopathy) and rhabdomyolysis. Finally, physicians should focus on preventing future episodes using patient education and instruction in self-monitoring.

InternalMed_Harrison

HYPERGLYCEMIC HYPEROSMOLAR STATE Clinical Features The prototypical patient with HHS is an elderly individual with type 2 DM, with a several-week history of polyuria, weight loss, and diminished oral intake that culminates in mental confusion, lethargy, or coma. The physical examination reflects profound dehydration and hyperosmolality and reveals hypotension, tachycardia, and altered mental status. Notably absent are symptoms of nausea, vomiting, and abdominal pain and the Kussmaul respirations characteristic of DKA. HHS is often precipitated by a serious, concurrent illness such as myocardial infarction or stroke. Sepsis, pneumonia, and other serious infections are frequent precipitants and should be sought. In addition, a debilitating condition (prior stroke or dementia) or social situation that compromises water intake usually contributes to the development of the disorder.

How to prevent and treat pharmacological hypoglycemias.

A 58 year-old woman with type 2 diabetes diagnosed 3 years before came to our clinic. Her treatment was metformin 850 mg every 12 hours and glimepiride 4 mg every 24 hours. After the initiation of glimepiride 9 months before her weight has increased 5 kg, and she suffers frequent hypoglycemias which have affected her while driving. Her BMI is 35.5 kg/m². She has a normal eye fund exam. She has hypertension treated with telmisartán and hidroclorotiazide with adequate control, and also hypercholesterolemia treated with atorvastatine 40 mg every 24 hours. Her blood test shows an HbA1c of 7.0%, normal values of microalbuminuria, total cholesterol 149 mg/dl, HDL cholesterol 52 mg/dl, LDL cholesterol 98 mg/dl and triglycerides 123 mg/dl. Her blood pressure is 129/81 mmHg, there was no orthostatic hypotension, and her peripheral neurological examination shows normal results. In summary, our case is a young woman with type 2 diabetes and obesity, without chronic complications and which has frequent hypoglycaemia. How must this woman be evaluated and treated?

Central pontine myelinolysis during treatment of hyperglycemic hyperosmolar syndrome: a case report.

Central pontine myelinolysis (CPM) is a non-inflammatory demyelinating lesion of the pons. CPM and extrapontine demyelination (EPM) are together termed osmotic demyelination syndrome (ODS), a known and serious complication of acute correction of hyponatremia. Conversely, hyperglycemic hyperosmolarity syndrome (HHS) develops in patients with type 2 diabetes who still have some insulin secretory ability due to infection, non-compliance with treatment, drugs, and coexisting diseases, and is often accompanied by ketosis. HHS represents a life-threatening endocrine emergency (mortality rate, 10-50%) associated with marked hyperglycemia and severe dehydration. HHS may develop ODS, and some cases have been associated with hypernatremia. The patient was an 87-year-old woman with hyperglycemia, dehydration, malnutrition, and potential thrombus formation during long-term bed rest. HHS was suspected to have developed due to progression of hyperglycemia and dehydration caused by pneumonia. Furthermore, ketoacidosis developed from ketosis and prerenal renal failure associated with circulating hypovolemia shock, which was also associated with disseminated intravascular coagulation. Treatment was started with continuous intravenous injection of fast-acting insulin and low-sodium replacement fluid. In addition, ceftriaxone sodium hydrate, heparin sodium, thrombomodulin α, human serum albumin, and dopamine hydrochloride were administered. Blood glucose, serum sodium, serum osmolality, and general condition (including vital, infection/inflammatory findings, and disseminated intravascular coagulation) improved promptly, but improvements in disturbance of consciousness were poor. Diffusion-weighted imaging of the brain 72 h after starting treatment showed no obvious abnormalities, but high-intensity signals in the midline of the pons became apparent 30 days later, leading to definitive diagnosis of CPM. Fluctuation of osmotic pressure by treatment from hyperosmolarity due to hyperglycemia and hypernatremia in the presence of risk factors such as malnutrition, severe illness, and metabolic disorders may be a cause of CPM onset. When treating HHS with risk factors, the possibility of progression to ODS needs to be kept in mind.

List of ICD-9 codes 240–279: endocrine, nutritional and metabolic diseases, and immunity disorders

Diseases of other endocrine glands (249–259) Note: for 249–259, the following fifth digit can be added: (250.x0) Diabetes mellitus type 2 (250.x1) Diabetes mellitus type 1 (250.x2) Diabetes mellitus type 2, uncontrolled (250.x3) Diabetes mellitus type 1, uncontrolled Secondary diabetes mellitus Secondary diabetes mellitus without mention of complication Secondary diabetes mellitus with ketoacidosis Secondary diabetes mellitus with hyperosmolarity Secondary diabetes mellitus with other coma Secondary diabetes mellitus with renal manifestations Secondary diabetes mellitus with ophthalmic manifestations Secondary diabetes mellitus with neurological manifestations Secondary diabetes mellitus with peripheral circulatory disorders Secondary diabetes mellitus with other specified manifestations Secondary diabetes mellitus with unspecified complications Diabetes mellitus Diabetes mellitus without mention of complication Diabetes with ketoacidosis

Diabetic coma

In the early to middle stages of ketoacidosis, patients are typically flushed and breathing rapidly and deeply, but visible dehydration, pale appearance from diminished perfusion, shallower breathing, and a fast heart rate are often present when coma is reached. However these features are variable and not always as described. If the patient is known to have diabetes, the diagnosis of diabetic ketoacidosis is usually suspected from the appearance and a history of 1–2 days of vomiting. The diagnosis is confirmed when the usual blood chemistries in the emergency department reveal a high blood sugar level and severe metabolic acidosis. Treatment of diabetic ketoacidosis consists of isotonic fluids to rapidly stabilize the circulation, continued intravenous saline with potassium and other electrolytes to replace deficits, insulin to reverse the ketoacidosis, and careful monitoring for complications.

Complications of diabetes

Nonketotic hyperosmolar coma (HNS) is an acute complication sharing many symptoms with DKA, but an entirely different origin and different treatment. A person with very high (usually considered to be above 300 mg/dl (16 mmol/L)) blood glucose levels, water is osmotically drawn out of cells into the blood and the kidneys eventually begin to dump glucose into the urine. This results in loss of water and an increase in blood osmolarity. If fluid is not replaced (by mouth or intravenously), the osmotic effect of high glucose levels, combined with the loss of water, will eventually lead to dehydration. The body's cells become progressively dehydrated as water is taken from them and excreted. Electrolyte imbalances are also common and are always dangerous. As with DKA, urgent medical treatment is necessary, commonly beginning with fluid volume replacement. Lethargy may ultimately progress to a coma, though this is more common in type 2 diabetes than type 1. Hypoglycemia

Pathology_Robbins

Type 2 diabetes also may manifest with polyuria and polydipsia. In some cases, medical attention is sought because of unexplained weakness or weight loss. Most frequently, however, the diagnosis is made after routine blood or urine testing in asymptomatic individuals. In the decompensated state, patients with type 2 diabetes may develop hyperosmolar nonketotic coma. This syndrome is engendered by severe dehydration resulting from sustained osmotic diuresis and urinary fluid loss due to chronic hyperglycemia. Typically, the affected individual is an older adult diabetic who is disabled by a stroke or an infection and is unable to maintain adequate water intake. The absence of ketoacidosis and its symptoms (nausea, vomiting, respiratory difficulties) delays recognition of the seriousness of the situation until the onset of severe dehydration and coma.


The treatment of choice for Clostridioides difficile infection is vancomycin orally 125mg/6h for 10 days. Metronidazole has been relegated to situations where vancomycin is not available.

Patient diagnosed with acute diverticulitis, treated with amoxicillin/clavulanic acid. After 5 days he starts with fever and diarrhea. He was diagnosed with Clostridium difficile colitis, amoxicillin/clavulanic acid was discontinued and metronidazole was prescribed. After 4 days he has not responded to metronidazole, but is clinically stable. The next step of treatment is:

Change metronidazole for oral vancomycin (125 mg, four times a day for 10 days).

Change metronidazole to piperacillin/ tazobactam (4 g piperacillin/0.5 g tazobactam every 8 hours).

Loop ileostomy with antegrade polyethylene glycol lavage.

Acute fulminant pseudomembranous colitis which developed after ileostomy closure and required emergent total colectomy: a case report.

Pseudomembranous colitis is known to be caused by Clostridium difficile; and, in 3% to 8% of patients, it lapses into an aggressive clinical course that is described as fulminant. We present here a case of extremely rapid and fatal fulminant pseudomembranous colitis that developed after ileostomy closure, a minor surgical procedure. To the best of our knowledge, this is the first case report of fatal fulminant pseudomembranous colitis after closure of a diversion ileostomy in an adult. A 69-year-old Japanese man, who had previously undergone low anterior resection and creation of a diverting ileostomy for stage III rectal carcinoma was admitted for ileostomy closure. Preoperatively, he received oral kanamycin and metronidazole along with parenteral cefmetazole. His surgery and postoperative course were uneventful until the third postoperative day, when fever and watery diarrhea became apparent. The next day he presented with epigastric and left lower abdominal pain. Computed tomography revealed a slightly distended colon. Later that night, his blood pressure fell and intravenous infusion was started. In the early morning of the fifth postoperative day, his blood pressure could be maintained only with a vasopressor. Follow-up computed tomography demonstrated severe colonic dilation. A colonoscopy confirmed the presence of pseudomembranous colitis, and so oral vancomycin was administered immediately. However, within three hours of the administration, his condition rapidly deteriorated into shock. Although an emergent total colectomy with creation of an end ileostomy was performed, our patient died 26 hours after the surgery. The histopathological examination was consistent with pseudomembranous colitis. It is important to recognize that, although rare, there is a type of extremely aggressive pseudomembranous colitis in which the usual waiting period for medical treatment might be lethal. We consider that colonoscopy and computed tomography are helpful to decide the necessity of emergent surgical treatment without delay.

[Clostridium difficile infection in a Department of Internal Medicine. A consecutive series of 45 patients].

A retrospective study of 45 patients with Clostridium difficile infection over a 4-year period in a department of Internal Medicine. Mean age was 79 years; sex-ratio (F/M)=1.5; 38% of the patients had neurological or severe psychiatric disorders; 20% had a neoplastic disease. Ninety-three percent of cases had received one or more antibiotics before onset of diarrhea, prescribed mainly for a pulmonary infection. Amoxicillin clavulanic acid and cephalosporins were the most frequently used treatments, respectively in 48% and 40% of cases. For 25 patients (56%) Clostridium difficile-associated diarrhea was considered as a nosocomial infection, and as community-acquired diarrhea in 20 cases (44%). Treatment included isolation of the patient as soon as bacteriological diagnosis was known and specific therapy was instituted by metronidazole or vancomycin for a mean of 18 days. The addition of Saccharomyces boulardii was used in of cases. The clinical course was rapidly favorable for 80% of patients. Five patients died with complications of severe colitis in 2 cases. Mean hospital stay was 49 days (annual mean of the department=10 days). Clostridium difficile diarrhea concerns above all elderly patients with one or more underlying pathologies. Amoxicillin clavulanic acid and third-generation cephalosporins are the most frequently prescribed antibiotics in these cases and have the highest correlation with this infectious complication. This medical problem requires greater knowledge as it causes significant morbidity and increases the risk of prolonged hospital stays.

Determining the optimal surgical timing of fulminant Clostridium difficile colitis by using four objective factors and computed tomography findings: A case report.

Clostridium difficile colitis is increasingly seen in everyday clinical situations, and most cases are treated with antibiotics. Fulminant C. difficile colitis (FCDC) is rare; however, it is extremely virulent, and understanding its appropriate surgical treatment is critical. The surgical timing is controversial because of the lack of concrete decision-making factors. We report a case of FCDC with a favourable outcome, which was achieved by using four objective factors and computed tomography (CT) findings. A patient with head trauma developed pneumonia at 2 days post-admission. He was prescribed with antibiotics. Fever and leucocytosis persisted on hospital day 10. Clostridium was detected in the stool on day 12, and metronidazole was administered. His condition did not improve; thus, he was started on vancomycin on day 14. The marked deterioration in the four laboratory parameters (white blood cell, albumin [Alb], creatinine, and body temperature) on day 15 and CT findings contributed to the decision to perform emergency subtotal colectomy and ileostomy. His condition improved dramatically postoperatively. Many factors of FCDC are already suggested for surgical intervention in the guidelines; however, they are often seen at the late stage of FCDC. Early detection of FCDC is the key to favourable surgical outcome. Following the trend of these objective factors guides in making appropriate surgical decisions. Focusing on the four objective factors and CT findings of FCDC could help surgeons detect FCDC at an early stage and decide the optimal surgical timing.

[Probiotic therapy of pseudomembranous colitis. Combination of intestinal lavage and oral administration of Escherichia coli].

An 82-year-old woman was admitted because of acute left heart failure with pulmonary oedema. There was a right basal pneumonia with congestion which was treated with amoxycillin and clavulanic acid. Severe watery diarrhoea with more than 10 stools daily occurred. Clostridium difficile was not isolated. Coloscopy as far as the right flexure revealed proximally increasing whitish coatings, like those in severe pseudomembranous colitis (PMC), revealed as acute erosive colitis histologically. The plate-like incomplete erosions contained fibrin and granulocyte deposits so typical of PMC. Clostridium difficile could again not be demonstrated. As intestinal lavage, already undertaken in preparation of the coloscopy, markedly improved the symptoms it was repeated for therapeutic purposes. This brought about further improvement and a fall in granulocyte count from 29,500 G/l to 10,700 G/l. Subsequently live E. coli bacteria (nissle 1917 strain) were administered. After 5 days stool frequency had fallen to one or two daily, each soft or partly formed. Stools were normal after a further week. Coloscopy 3 weeks after onset of treatment showed almost complete healing of the PMC. The successful treatment of PMC with intestinal lavage and physiological E. coli administration agrees with the results of animal experiments and clinical experience. Whether it is an effective alternative to primary standard treatment with vancomycin or metronidazole remains to be tested by further experience, preferably properly controlled therapeutic trials.

Acute Diverticulitis -- Treatment / Management

Upon clinical presentation, acute diverticulitis can be managed with either outpatient or inpatient care. According to American Society of Colon and Rectal Surgeons, a patient who cannot tolerate oral intake, is excessively vomiting, shows signs of peritonitis, is immunocompromised, or at an advanced age should be hospitalized. In the absence of these conditions, and if appropriate prompt follow-up can be established, acute diverticulitis can be managed on an outpatient basis. It is reported that success rate of outpatient management is about 94% to 97%. The standard of outpatient care includes bowel rest, increase fluid intake, and oral antibiotic therapy (single or multiple drug regimen) that covers gram-negative rods and anaerobic bacteria. The most common regimen used in the United States consists of quinolones (ciprofloxacin) or sulfa drugs (trimethoprim/sulfamethoxazole) in combination with metronidazole  (or clindamycin, if the patient is intolerant to metronidazole) or single agent amoxicillin-clavulanate for 7 to 10 days. [8] [3] [9]

Colon Diverticulitis -- Treatment / Management

The medical management of acute non-complicated diverticulitis includes oral or intravenous antibiotics, pain control, hydration, and restricted oral intake. Medical management of diverticulitis with antibiotics remains the standard of care. However, antibiotic choice, duration of treatment, and route of administration remain controversial. [18] Most cases of uncomplicated diverticulitis are successfully treatable in the outpatient setting. Oral antibiotics, such as ciprofloxacin and metronidazole or amoxicillin-clavulanate, are prescribed for 7 to 10 days with recommendations to minimize oral intake until the pain has resolved. [15]

Antibiotic Regimen after a Total Abdominal Colectomy with Ileostomy for Fulminant Clostridium difficile Colitis: A Multi-Institutional Study.

Fulminant Clostridium difficile colitis (fCDC) is a highly lethal disease with mortality rates ranging between 12% and 80%. Although often these patients require a total abdominal colectomy (TAC) with ileostomy, there is no established management protocol for post-operative antibiotics. In this study we aim to make some recommendations for post-operative antibiotic usage, while describing the practice across different institutions. Multi-institutional retrospective case series including fCDC patients who underwent a TAC between January 1, 2007, and June 30, 2012. We first analyzed the complete cohort and consecutively performed a survivor analysis, comparing different antibiotic regimens. Additionally we stratified by time interval (antibiotics for ≤7 d, or ≥8 d). Primary outcome was in-hospital mortality. Additional secondary outcomes included hospital length of stay (HLOS), ICU LOS, number of ventilator-free days, and occurrence of intra-abdominal complications (proctitis, abscess, sepsis, etc.). A total of 100 fCDC patients that underwent a TAC were included across five institutions. Four different antibiotic regimens were compared; A (metronidazole IV+vancomycin PO), B (metronidazole IV), C (metronidazole IV+vanco PO and PR), and D (metronidazole IV+vancomycin PR). The combination of IV metronidazole with or without PO vancomycin showed superior outcomes in terms of a shorter ICU length of stay and more ventilator-free days. However, when comparing metronidazole alone vs. metronidazole and any combination of vancomycin, no significant differences were found. Neither the addition of vancomycin enema, nor the time interval changed outcomes. Patients, after a TAC for fCDC, may be placed on either IV metronidazole or PO vancomycin depending upon local antibiograms, and proctitis may be treated with the addition of a vancomycin enema (PR). There was no data to support routine treatment of more than 7 d.

[Antibiotic-associated pseudomembranous colitis: retrospective study of 48 cases diagnosed by colonoscopy].

Pseudomembranous colitis (PMC) is a rare but potentially severe complication of antibiotic treatment, which is characterized by the proliferation of the bacterium Clostridium difficile in the colon. In this retrospective study, 48 cases of endoscopically confirmed PMC were included. The following variables were analysed: characteristics of the patients, antibiotics, clinical, biological and endoscopic features of PMC and its treatment. The antibiotic treatment was often ambulatory (83 per cent) for a broncho-pulmonary infection (42 per cent). In 90 per cent of the cases, the treatment included a -lactam, frequently amoxicillin with clavulanic acid, and in 25 per cent of the cases, a fluoroquinolone. The PMC generally occurred after more than 4 days of treatment and was associated with diarrhoea, abdominal pain, fever and rarely vomiting (23 per cent). The complications were hypokalaemia (37 per cent), renal failure (27 per cent) and/or hypoproteinaemia (50 per cent). Pseumembranes were found between the rectum and the left angle of the colon. All patients recovered after one week of oral treatment with metronidazole and/or vancomycin, often in association with Saccharomyces boulardii.

WHO Model List of Essential Medicines

Antischistosomals and other antinematode medicines Praziquantel Triclabendazole Oxamniquineα Cysticidal medicines Albendazoleα Mebendazoleα Praziquantelα Antibacterials Access group antibiotics Amikacin Amoxicillin Amoxicillin/clavulanic acid (amoxicillin + clavulanic acid) Ampicillin Benzathine benzylpenicillin Benzylpenicillin Cefalexin Cefazolin Chloramphenicol Clindamycin Cloxacillin Doxycycline Gentamicin Metronidazole Nitrofurantoin Phenoxymethylpenicillin (penicillin V) Procaine benzylpenicillin Spectinomycin Sulfamethoxazole/trimethoprim (sulfamethoxazole + trimethoprim) Trimethoprim Watch group antibiotics Azithromycin Cefixime Cefotaxime Ceftriaxone Cefuroxime Ciprofloxacin Clarithromycin Piperacillin/tazobactam (piperacillin + tazobactam) Vancomycin Ceftazidimeα Meropenemα Vancomycinα

WHO Model List of Essential Medicines for Children

Antifilarials Albendazole Diethylcarbamazine Ivermectin Antischistosomals and other antinematode medicines Praziquantel Triclabendazole Oxamniquine Antibiotics Access group antibiotics Amikacin Amoxicillin Amoxicillin/clavulanic acid (amoxicillin + clavulanic acid) Ampicillin Benzathine benzylpenicillin Benzylpenicillin Cefalexin Cefazolin Chloramphenicol Clindamycin Cloxacillin Doxycycline Gentamicin Metronidazole Nitrofurantoin Phenoxymethylpenicillin (penicillin V) Procaine benzylpenicillin Sulfamethoxazole/trimethoprim (sulfamethoxazole + trimethoprim) Watch group antibiotics Azithromycin Cefixime Cefotaxime Ceftriaxone Cefuroxime Ciprofloxacin Clarithromycin Piperacillin/tazobactam (piperacillin + tazobactam) Vancomycin Ceftazidime Meropenem Vancomycin Reserve group antibiotics Ceftazidime/avibactam (ceftazidime + avibactam) Colistin Fosfomycin Linezolid Polymyxin B Antileprosy medicines Clofazimine Dapsone Rifampicin

Cholecystitis

Other Supportive measures may be instituted prior to surgery. These measures include fluid resuscitation. Intravenous opioids can be used for pain control. Antibiotics are often not needed. If used they should target enteric organisms (e.g. Enterobacteriaceae), such as E. coli and Bacteroides. This may consist of a broad spectrum antibiotic; such as piperacillin-tazobactam, ampicillin-sulbactam, ticarcillin-clavulanate (Timentin), a third generation cephalosporin (e.g.ceftriaxone) or a quinolone antibiotic (such as ciprofloxacin) and anaerobic bacteria coverage, such as metronidazole. For penicillin allergic people, aztreonam or a quinolone with metronidazole may be used.

Ranitidine bismuth citrate

Inside, regardless of food intake, 2 times a day (morning and evening). In the treatment and prevention of benign gastric and duodenal ulcers, as well as for the eradication of Helicobacter pylori and the relief of concomitant symptoms of dyspepsia, the following combination therapy regimens are used. Within 7 days - 3 drugs: Scheme 1. 2 times a day - ranitidine bismuth citrate 400 mg, clarithromycin 500 mg, metronidazole 400 mg or amoxicillin 1 g. Scheme 2. 2 times a day - ranitidine bismuth citrate 400 mg, clarithromycin 250 mg, metronidazole 400 or 500 mg or tinidazole 500 mg. Scheme 3. Ranitidine bismuth citrate 400 mg 2 times a day, metronidazole 500 mg 3 times a day, tetracycline 500 mg 4 times a day. Scheme 4. 2 times a day - ranitidine bismuth citrate 400 mg, tinidazole 500 mg, amoxicillin 1 g. Within 14 days - 2 drugs: Scheme 5. Ranitidine bismuth citrate 400 mg 2 times a day and clarithromycin 500 mg 2 or 3 times a day. Scheme 6. Ranitidine bismuth citrate 400 mg 2 times a

Outpatient treatment in uncomplicated acute diverticulitis: 5-year experience.

Most cases of diverticular inflammation are mild and require only medical treatment with liquid diet and antibiotics. Until recently, this treatment required admission to hospitals, which consequently entailed costs. In most cases, treatment was conservative, and less than a quarter of patients admitted actually underwent surgery. In the last year, the outpatient treatment of these patients with uncomplicated diverticulitis has proven effective and safe. The aim of the present study was to describe our experience after 5 years of outpatient treatment with oral antibiotics. We conducted a retrospective revision study between January 2010 and December 2014. We included all patients admitted to the Emergency Department of the University General Hospital of Elche with a diagnosis of uncomplicated acute diverticulitis based on medical history, physical examination and abdominopelvic computed tomography (CT) scanning. Outpatient treatment consisted of oral antibiotics for 10 days (metronidazole 500 mg/8 h and ciprofloxacin 500 mg/12 h), a liquid diet and oral analgesics (acetaminophen 1 g/6 h). During the period from January 2010 to December 2014, 224 patients were treated on an outpatient basis at a success rate of over 92%. Only 18 patients (8%) required admission after outpatient treatment. Outpatient treatment of uncomplicated acute diverticulitis was demonstrated to be safe and effective.

Tolevamer

History Termination of development In early 2008, a noninferiority study versus vancomycin or metronidazole for Clostridium difficile associated diarrhea (CDAD) found that about half of the patients in the tolevamer group did not complete the treatment, versus 25% in the vancomycin and 29% in the metronidazole groups. CDAD recurrence in patients reaching clinical success was reduced significantly by tolevamer (6% recurrence rate), vancomycin (18%) and metronidazole (19%). However, the good result of tolevamer is partly due to the high drop-out rate in this group. Since tolevamer did not reach its primary endpoint in this study, its development was halted. References Antidiarrhoeals Sulfonic acids

Piperacillin/tazobactam compared with cefuroxime/ metronidazole in the treatment of intra-abdominal infections.

To assess the effect of piperacillin/tazobactam compared with cefuroxime/metronidazole in the treatment of patients with intra-abdominal infections. Randomised open study. 16 Swedish and 6 Norwegian hospitals. 269 patients with intra-abdominal infections were randomised and treated with at least one dose of each study drug. 205 patients, 105 treated with piperacillin/tazobactam and 100 with cefuroxime, were clinically evaluable for follow up (had been given the full course of treatment). Patients were given piperacillin 4g/tazobactam 0.5 g every 8 hours or cefuroxime 1.5 g every 8 hours plus metronidazole 1.5 g every 24 hours. Each patient was to be treated for a minimum of 3 days and not more than 10 days. Clinical evaluation of infection at the end of and 4-6 weeks after treatment. Evaluation of safety and tolerance to the drugs and bacteriological susceptibility to the treatment drugs. In the intention to treat analysis treatment was equally successful for piperacillin/ tazobactam (103/140, 74%) and the cefuroxime/metronidazole groups (90/129, 70%) (p = 0.6). Corresponding figures for the clinically evaluable group were 102/105 (97%) and 94/100 (94%) for piperacillin/tazobactam and cefuroxime/metronidazole groups, respectively, at the end of treatment. At late follow up, 92/105 (88%) and 83/100 (83%) in the two groups, respectively, remained free of infection. The side effects of the treatment were mild and evenly distributed between the two groups. Most pathogens were susceptible to the drugs in both treatment groups. Both piperacillin/tazobactam and cefuroxime/metronidazole are well suited to the treatment of patients with intra-abdominal infections, and we found no significant difference between the two. The drugs were safe and well tolerated in the regimens used.

Management of uncomplicated acute diverticulitis: results of a survey.

A survey was conducted to document current medical treatment of patients with uncomplicated acute diverticulitis. A survey was mailed to 667 fellows of The American Society of Colon and Rectal Surgeons certified by the American Board of Colon and Rectal Surgery. Queries were based on a clinical scenario of a patient with uncomplicated diverticulitis. Three hundred seventy-three surveys (56 percent) were returned completed. The majority (66 percent) chose an abdominal computed tomographic scan as the initial diagnostic test. One-half used a single intravenous antibiotic with second-generation cephalosporins (27 percent) and ampicillin/sulbactam (16 percent) being the most common. Oral antibiotics given at discharge were ciprofloxacin (18 percent), amoxicillin/clavulanate (14 percent), metronidazole (7 percent), and doxycycline (6 percent). Combinations chosen were ciprofloxacin/metronidazole (28 percent) and metronidazole/trimethoprim sulfamethoxazole (6 percent), whereas 21 percent chose a variety of other antibiotics. The majority (74 percent) prescribed oral antibiotics for 7 to 10 days. Dietary recommendations at discharge were low residue (68 percent), regular (21 percent), and high residue (10 percent). Half of those surveyed believed avoidance of seeds and nuts were of no value. Follow-up examinations chosen included sigmoidoscopy and barium enema (29 percent), colonoscopy (25 percent), sigmoidoscopy (17 percent), barium enema (13 percent), and other (16 percent). Sixty-five percent of colon and rectal surgeons claim to handle more than half of their patients with uncomplicated diverticulitis on an outpatient basis. Variations in the management of uncomplicated sigmoid diverticulitis are noted among colon and rectal surgeons, especially in terms of antibiotic choice, discharge instructions, and follow-up outpatient studies. The survey results are compared with the conclusions reached in The American Society of Colon and Rectal Surgeons practice parameters. Documentation of practice pattern variation may serve as an educational tool for physicians to improve their quality and cost of medical care. Consideration should be given to better publicize already existing American Society of Colon and Rectal Surgeons practice parameters for this common entity.

Anaerobic infection

The available parenteral antimicrobials for most infections are metronidazole, clindamycin, chloramphenicol, cefoxitin, a penicillin (i.e. ticarcillin, ampicillin, piperacillin) and a beta-lactamase inhibitor (i.e. clavulanic acid, sulbactam, tazobactam), and a carbapenem (imipenem, meropenem, doripenem, ertapenem). An antimicrobial effective against Gram-negative enteric bacilli (i.e. aminoglycoside) or an anti-pseudomonal cephalosporin (i.e. cefepime ) are generally added to metronidazole, and occasionally cefoxitin when treating intra-abdominal infections to provide coverage for these organisms. Clindamycin should not be used as a single agent as empiric therapy for abdominal infections. Penicillin can be added to metronidazole in treating of intracranial, pulmonary and dental infections to provide coverage against microaerophilic streptococci, and Actinomyces.

Update on the management of uncomplicated acute diverticulitis at our centre. Equally effective, more efficient.

The current trend in the treatment of non-complicated diverticulitis is the outpatient management with antibiotic or even anti-inflammatory regimens in selected cases. We present a comparison of the results in our hospital with different protocols applied in 2016 and 2017. All patients selected for this study were diagnosed with diverticulitis grade Ia of Hinchey's classification according to radiological findings on abdominal CT. We have analyzed two retrospective cohorts: 100 patients treated in 2016 according to the old protocol and 104 patients treated in 2017 with a new protocol. In 2016, the candidates for ambulatory treatment remained under observation for 24 hours before being discharged. The treatment consisted of 14 days of ciprofloxacin and metronidazole. In 2017, only patients with more acute symptoms were observed 24 hours and amoxicillin-clavulanic acid was prescribed for only 5 days. The persistence of the disease in 2016 was 6% and in 2017 was only 5.77% (p = 0.944). Recurrence during the first year was 13% in the first group, while in the second it was 5.7%, although this difference was not statistically significant. Likewise, a significant reduction in health costs was achieved. Outpatient treatment of acute uncomplicated diverticulitis with oral treatment seems to be a safe and effective therapeutic strategy in selected patients with low comorbidity.

Peritonsillar abscess

Diagnosis Diagnosis is usually based on the symptoms. Medical imaging may be done to rule out complications. Medical imaging may include CT scan, MRI, or ultrasound is also useful in diagnosis. Treatment Medical treatment with antibiotics, volume repletion with fluids, and pain medication is usually adequate, although in cases where airway obstruction or systemic sepsis occurs, surgical drainage may be necessary. Steroids may also be useful. Admission to hospital is generally not needed. Medication The infection is frequently penicillin resistant. There are a number of antibiotics options including amoxicillin/clavulanate, clindamycin, or metronidazole in combination with benzylpenicillin (penicillin G) or penicillin V. Piperacillin/tazobactam may also be used.

Flare-Up Diverticulitis in the Terminal Ileum in Short Interval after Conservative Therapy: Report of a Case.

Diverticulitis in the terminal ileum is uncommon. Past reports suggested that conservative therapy may be feasible to treat terminal ileum diverticulitis without perforation; however, there is no consensus on the therapeutic strategy for small bowel diverticulitis. We present a 37-year-old man who was referred to our hospital for sudden onset of abdominal pain and nausea. He was diagnosed with diverticulitis in the terminal ileum by computed tomography (CT). Tazobactam/piperacillin hydrate (18 g/day) was administered. The antibiotic treatment was maintained for 7 days, and the symptoms disappeared after the treatment. Thirty-eight days after antibiotic therapy, he noticed severe abdominal pain again. He was diagnosed with diverticulitis in terminal ileum which was flare-up of inflammation. He was given antibiotic therapy again. Nine days after antibiotic therapy, laparoscopy assisted right hemicolectomy and resection of 20 cm of terminal ileum were performed. Histopathology report confirmed multiple ileal diverticulitis. He was discharged from our hospital 12 days after the surgery. Colonoscopy was performed two months after the surgery and it revealed no finding suggesting inflammatory bowel disease. Surgical treatment should be taken into account as a potential treatment option to manage the diverticulitis in the terminal ileum even though it is not perforated.

Polymicrobial bacteraemia with Clostridioides difficile and Pseudomonas aeruginosa in an elderly man following antibiotic use.

<iClostridioides difficile</i is a micro-organism well known to cause pseudomembranous colitis with rare extraintestinal manifestations. We present the case of an elderly male with multiple comorbidities who presented with acute onset of fever/chills and hypotension, found to have polymicrobial bacteraemia with <iC. difficile</i and <iPseudomonas aeruginosa</i He was treated with piperacillin/tazobactam for <iP. aeruginosa</i bacteraemia, oral vancomycin for <iC. difficile</i colitis and intravenous, followed by oral metronidazole for <iC. difficile</i bacteraemia. <iPseudomonas</i cleared after 1 day, and <iClostridioides</i cleared after 4 days. Following an initial septic presentation, he responded appropriately to antimicrobial therapy and did well in follow-up.

[Therapeutic and prophylactic role of mesalazine (5-ASA) in symptomatic diverticular disease of the large intestine. 4 year follow-up results].

In order to evaluate the efficacy and tolerability of mesalazine (5-ASA) in the prophylaxis of symptomatic relapses, of major complications and of microhemorrhagic phenomena in diverticular disease of the large intestine (MDC), prospective clinical study was conducted on patients with light-moderate symptomatic MDC under treatment with sulbactam-ampicillin 1.5 g/12 h i.m. and rifaximine 400 mg/12 h per os for 7 days. Follow-up period of 5 years with seriated checkups and laboratory and instrumentation controls. End points are represented by the relapse on inflammation and/or by the occurrence of major complications. On enrollment, 166 patients were randomized to receive mesalazine (Pentacol tablets--SOFAR S.p.A.) 400 mg b.i.d. per os for 8 weeks (81 patients; group M) or no supplementary treatment (85 patients; group C). After 4 years of follow-up, 44 patients dropped out of the study (9 because of major complications, 3 for massive hemorrhage, and 32 drop outs). Symptomatic relapses occurred in 51 patients (12 M; 39 C), while minor diverticular hemorrhages occurred in 43 patients (12 M; 31 C), with an estimated probability of remaining free respectively from symptomatic relapse (p=0.00005) and from microhemorrhagic phenomena (p=0.001) decisively in favor of the group treated with mesalazine. The duration of abdominal pain due to diverticolitis was also shorter in patients of group M (p=0.0002), while the incidence of major complications and side effects was comparable in the two groups. In conclusion, supplementary treatment with mesalazine in patients affected with MDC--at a follow-up limited to 48 months--proved to be well tolerated and effective in reducing the frequency of symptomatic relapses and microhemorrhagic phenomena and in reducing the duration of abdominal pain.

Antimicrobial resistance in Clostridioides (Clostridium) difficile derived from humans: a systematic review and meta-analysis.

Clostridioides (Clostridium) difficile is an important pathogen of healthcare- associated diarrhea, however, an increase in the occurrence of C. difficile infection (CDI) outside hospital settings has been reported. The accumulation of antimicrobial resistance in C. difficile can increase the risk of CDI development and/or its spread. The limited number of antimicrobials for the treatment of CDI is matter of some concern. In order to summarize the data on antimicrobial resistance to C. difficile derived from humans, a systematic review and meta-analysis were performed. We searched five bibliographic databases: (MEDLINE [PubMed], Scopus, Embase, Cochrane Library and Web of Science) for studies that focused on antimicrobial susceptibility testing in C. difficile and were published between 1992 and 2019. The weighted pooled resistance (WPR) for each antimicrobial agent was calculated using a random- effects model. A total of 111 studies were included. The WPR for metronidazole and vancomycin was 1.0% (95% CI 0-3%) and 1% (95% CI 0-2%) for the breakpoint > 2 mg/L and 0% (95% CI 0%) for breakpoint ≥32 μg/ml. Rifampin and tigecycline had a WPRs of 37.0% (95% CI 18-58%) and 1% (95% CI 0-3%), respectively. The WPRs for the other antimicrobials were as follows: ciprofloxacin 95% (95% CI 85-100%), moxifloxacin 32% (95% CI 25-40%), clindamycin 59% (95% CI 53-65%), amoxicillin/clavulanate 0% (0-0%), piperacillin/tazobactam 0% (0-0%) and ceftriaxone 47% (95% CI 29-65%). Tetracycline had a WPR 20% (95% CI 14-27%) and meropenem showed 0% (95% CI 0-1%); resistance to fidaxomicin was reported in one isolate (0.08%). Resistance to metronidazole, vancomycin, fidaxomicin, meropenem and piperacillin/tazobactam is reported rarely. From the alternative CDI drug treatments, tigecycline had a lower resistance rate than rifampin. The high-risk antimicrobials for CDI development showed a high level of resistance, the highest was seen in the second generation of fluoroquinolones and clindamycin; amoxicillin/clavulanate showed almost no resistance. Tetracycline resistance was present in one fifth of human clinical C. difficile isolates.

Febrile neutropenia

In 2010, updated guidelines were issued by the Infectious Diseases Society of America, recommending use of cefepime, carbapenems (meropenem and imipenem/cilastatin), or piperacillin/tazobactam for high-risk patients and amoxicillin-clavulanic acid and ciprofloxacin for low-risk patients. Patients who do not strictly fulfill the criteria of low-risk patients should be admitted to the hospital and treated as high-risk patients. Research to compare antibiotic treatments currently recommended in consensus guidelines identified 44 studies comparing different antibiotics. Significantly higher mortality was reported for cefepime compared to all other antibiotics combined. Piperacillin/tazobactam resulted in lower mortality than other antibiotics. Piperacillin/tazobactam might be the preferred antibiotic for the treatment of cancer patients with fever and neutropenia, while cefepime should not be used.

One-day versus four-day antibiotic treatment for acute right colonic uncomplicated diverticulitis: A randomized clinical trial.

Currently, right colonic uncomplicated diverticulitis is typically treated with antibiotic therapy. However, the optimal duration of treatment is unknown. The aim of the present study was to compare the treatment failure rates between 1- and 4-day antibiotic treatment protocols. A prospective randomized study in adults presenting with uncomplicated diverticulitis at the first episode from July 2011 to June 2014 was performed. Patients were randomized to receive intravenous antibiotics for 1 day (1-day group) or intravenous and oral antibiotics for 4 days (4-day group). All patients received cefmetazole and metronidazole. Treatment failure was defined as readmission within 30 days and disease recurrence during the follow-up period. Overall, 87 and 89 patients were randomized to the 1-day and 4-day groups, respectively. All patients were successfully treated initially. The hospital length of stay was shorter in the 1-day group than in the 4-day group (3.1 vs. 3.8 days, respectively; p<0.001). After discharge, there were no significant differences between the groups in treatment failure (15/87, 17.2% vs. 19/89, 21.3%; p=0.493). In each group, there were readmission within 30 days (9.2% vs. 12.4%; p=0.502) and recurrence over a median follow-up period of 32 months (10.3% vs. 9.0%; p=0.762). In 34 patients who experienced treatment failure, 6 required surgery. Single-day antibiotic treatment is as effective as 4-day therapy for the prevention of readmission and recurrence in patients with right colonic uncomplicated diverticulitis.

Evaluation of the in vitro activity of ertapenem and nine other comparator agents against 337 anaerobic bacteria.

Ertapenem activity in vitro was compared with that of nine reference antibiotics against 337 anaerobes by determining minimal inhibition concentrations (MICs). Amongst 246 Gram-negative anaerobes, 4, 8, 3, 4, 7, 2 and 52 strains showed resistance to ertapenem, amoxicillin/clavulanic acid, ticarcillin/clavulanic acid, piperacillin/tazobactam, cefoxitin, imipenem and clindamycin, respectively, and all strains were inhibited by metronidazole. Ertapenem MIC(50) values were 0.5, 0.25, 0.06 and <or=0.03mg/L for the Bacteroides fragilis group, Prevotella spp., fusobacteria and Gram-positive cocci, respectively. Overall resistance rates were 2.1%, 51.3%, 2.4%, 1.2%, 1.5%, 7.1%, 0.6%, 22% and 1.5% for ertapenem, amoxicillin, amoxicillin/clavulanic acid, ticarcillin/clavulanic acid, piperacillin/tazobactam, cefoxitin, imipenem, clindamycin and metronidazole, respectively. Ertapenem showed a broad spectrum and good activity against anaerobes.

[Safety and efficiency of ambulatory treatment of acute diverticulitis].

The treatment of acute diverticulitis is currently being modified, showing a tendency to limit surgical treatment and favor conservative management. To analyze the safety and efficiency of ambulatory treatment of acute diverticulitis in a selected group of patients. We performed a prospective study of domiciliary oral antibiotic therapy for acute diverticulitis in a cohort of patients in the Emergency Surgery Section of our hospital. Seventy-four patients (44 men and 30 women) were included between 2000 and 2006. Patients with Hinchey stage 1 diverticulitis and those with Hinchey stage 2 diverticulitis and abscesses of less than 3cm, who were clinically and biochemically stable, were selected. The patients were treated with oral ciprofloxacin and metronidazole for 7-10 days. Follow-up was performed in the outpatients unit with clinical evaluation at 10 days and an imaging test at 1 month. The mean age of the patients was 55 years. The most frequent clinical presentation was spontaneous abdominal pain associated with leukocytosis. The mean duration of treatment was 8.8 days. Four patients (5.4%) required subsequent hospital admission for intravenous antibiotic administration and 70 (94.6%) completed treatment without complications. During follow-up, two cases of colonic adenocarcinoma and six cases of polyposis were diagnosed. Only 13 patients underwent elective surgery. In most of the patients studied, ambulatory conservative management was safe and effective in the treatment of uncomplicated acute diverticulitis. Moreover, this approach reduces length of hospital stay and lowers costs.

Chorioamnionitis

Treatment The American College of Obstetricians and Gynecologists' Committee Opinion proposes the use of antibiotic treatment in intrapartum mothers with suspected or confirmed chorioamnionitis and maternal fever without an identifiable cause. Intrapartum antibiotic treatment consists of: Standard Ampicillin + gentamicin Alternative Ampicillin/sulbactam Ticarcillin/clavulanate Cefoxitine Cefotetan Piperacillin/tazobactam Ertapenem Cesarean delivery Ampicillin and gentamicin plus either clindamycin or metronidazole Penicillin-allergy Vancomycin + gentamicin Gentamicin + clindamycin

[A case of pseudomembranous enterocolitis which diagnosis was delayed in the outpatient clinic].

A 71-year-old male visited our hospital because of diarrhea. At first we suspected infectious colitis and levofloxacin (300 mg/day) was administered for four days. But the diarrhea continued, so performed a barium enema after about 3 weeks from onset. Round polyposis from the rectum to the sigmoid colon were found. Colonoscopy was suggested to the patient, but was rejected. However diarrhea continued and fever appeared. Ceftriaxone (1 g/day) and sparfloxacin (200 mg/day) were administered, but the symptoms increased. He was admitted about 6 weeks from onset, and the colonoscopy showed multiple round yellow-white pseudomembranes. Pseudomembranous enterocolitis diagnosed because Clostridium difficile and its toxin were positive in the feces. After oral administration of vancomycin (1.5 g/day) was started, the symptoms alleviated rapidly and disappearance of pseudomembrane was confirmed by colonoscopy.

Ludwig's angina

Antibiotics Antibiotic therapy is empirical, it is given until culture and sensitivity results are obtained. The empirical therapy should be effective against both aerobic and anaerobic bacteria species commonly involved in Ludwig's Angina. Only when culture and sensitivity results return should therapy be tailored to the specific requirements of the patient. Empirical coverage should consist of either a penicillin with a B-lactamase inhibitor such as amoxicillin/ticarcillin with clavulanic acid or a Beta-lactamase resistant antibiotic such as cefoxitin, cefuroxime, imipenem or meropenem. This should be given in combination with a drug effective against anaerobes such as clindamycin or metronidazole. Parenteral antibiotics are suggested until the patient is no longer febrile for at least 48 hours. Oral therapy can then commence to last for 2 weeks, with amoxicillin with clavulanic acid, clindamycin, ciprofloxacin, trimethoprim-sulfamethoxazole, or metronidazole.

Randomized controlled trial of oral vs intravenous therapy for the clinically diagnosed acute uncomplicated diverticulitis.

Despite the high prevalence of hospitalization for left iliac fossa tenderness, there is a striking lack of randomized data available to guide therapy. The authors hypothesize that an oral antibiotic and fluids are not inferior to intravenous (IV) antibiotics and 'bowel rest' in clinically diagnosed acute uncomplicated diverticulitis. A randomized controlled trial was constructed in two District General Hospitals. All clinically diagnosed patients presenting with acute uncomplicated diverticulitis were eligible for the study. Oral and IV regimens utilizing ciprofloxacin and metronidazole were compared. The primary outcomes studied were surrogates for resolution of symptoms (including tenderness on day 3 and length of stay) and failure of oral therapy. Secondary endpoints studied were serial constitutional and biomarker trends. There were 41 patients in the oral arm and 38 in the IV arm (n = 79). No patient had to be converted to IV antibiotics from the oral group. There was a complete resolution of symptoms in both groups. Tenderness was equivalent in both groups on day 3. Among secondary endpoints, a serial decrease in C reactive protein was the best serological predictor of resolution for both groups. Oral antibiotics are not inferior to intravenous antibiotics in achieving resolution of clinically diagnosed diverticulitis.

[Applicability, safety and efficacy of an ambulatory treatment protocol in patients with uncomplicated acute diverticulitis].

The aim of this study was to evaluate the applicability, safety and efficacy of an ambulatory treatment protocol in patients with uncomplicated acute diverticulitis. All patients diagnosed with uncomplicated acute diverticulitis based on abdominal computed tomography findings during a 2-year period were prospectively included. Patients with vomiting, severe comorbidities, or without an appropriate family environment were excluded. Ambulatory treatment consisted of oral antibiotics for 1 week (amoxicillin-clavulanic 1 g t.i.d. or ciprofloxacin 500 mg b.i.d. plus metronidazole 500 mg t.i.d. in patients with penicillin allergy). A clear liquid diet for the first 2 days and pain control with oral acetaminophen 1 g t.i.d. were also recommended. Fifty-three patients were diagnosed with uncomplicated acute diverticulitis and 13 patients were excluded. Therefore, ambulatory treatment was initiated in 40 patients. Only two patients (5%) required admission after outpatient therapy was started due to vomiting and persistent abdominal pain, respectively. In both patients, the inflammatory process was successfully resolved by intravenous antibiotic treatment. In the remaining 38 patients (95%), ambulatory treatment was completed without complications. Ambulatory treatment of uncomplicated acute diverticulitis is safe, effective and applicable in most patients with tolerance to oral intake and with an appropriate family environment.