The correct answer is 3. Easy question if pathology is suspected, which I also think is simple because the clinical description is textbook hypertrophic pyloric stenosis.

[HIDDEN] Easy question if pathology is suspected, which I also think is simple because the clinical description is textbook hypertrophic pyloric stenosis.

Child 28 days old, born at term. History of normal pregnancy and delivery. He has been breastfed since birth. He consults because 8 days ago he started vomiting, initially sporadically and since 5 days ago, after all feedings. He is permanently hungry. The vomiting is of "squirting" food content. On palpation, the abdomen is soft and depressible, without visceromegaly. The blood gas analysis showed pH 7.49, bicarbonate 30 mEq/l, pCO2 53 mmHg, base excess +8 mEq/l. Ions: Na 137 mEq/l, K 3.1 mEq/l, Cl 94 mEq/l. Taking into account the most probable diagnosis in the clinical picture described, what is the complementary test of choice to confirm this clinical diagnosis?

[Cystic fibrosis revealed by dehydration with hypochloronatremic alkalosis in 3 infants and a neonate].

BACKGROUND--Acute dehydration with hypochloronatremic metabolic alkalosis is a classical complication of cystic fibrosis of the pancreas. Its progressive development as a revealing manifestation of the disease is rare as is its appearance in newborns. Case n. 1.--A 13 month-old girl was admitted because of status epilepticus. She was severely dehydrated (20% weight loss) but had normal diuresis. Investigations showed metabolic alkalosis, hypochloronatremia and hypokalemia. All the manifestations disappeared within 5 days with treatment but three sweat tests were abnormal. Case n. 2.--A 7 month-old girl was admitted because she suffered from progressive loss of weight (10%); she was dehydrated and had metabolic alkalosis plus hypochloronatremia, but her diuresis was normal. Two sweat tests were abnormal. Case n. 3.--A 4.5 month-old boy was admitted because he suffered from severe (12%) weight loss. His diuresis was normal despite dehydration; metabolic alkalosis and hypochloronatremia were found. Two subsequent sweat tests were abnormal. Case n. 4.--A 3 day-old girl was admitted suffering from meconium ileus. Two initial mechanism analysis for protein were abnormal. She had a cardiorespiratory arrest on the 13th day of life, when she had lost 14% of her birth weight; investigations showed metabolic alkalosis, hyponatremia (83 mEq/l), hypochloremia (45 mEq/l); kalemia was 5.9 mEq/l. Peritoneal dialysis was needed to correct hydroelectrolytic changes. A sweat test performed on the 26th day of life was also abnormal. Investigations performed during the periods of dehydration, and repeated later, showed transient functional kidney failure. None of the four patients had any respiratory or gastrointestinal clinical manifestations of cystic fibrosis. CONCLUSION--Metabolic alkalosis with hypochloronatremia plus progressive, severe dehydration in infants whose diuresis is paradoxically normal must be followed by examination for cystic fibrosis.

Association of Bartter's syndrome and empty sella.

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.

Ringer's lactate solution

In a large-volume resuscitation over several hours, LRS maintains a more stable blood pH than normal saline. Chemistry One liter of Ringer's lactate solution contains: 130–131 mEq of sodium ion = 130 mmol L−1 109–111 mEq of chloride ion = 109 mmol L−1 28–29 mEq of lactate ion = 28 mmol L−1 4–5 mEq of potassium ion = 4 mmol L−1 2–3 mEq of calcium ion = 1.5 mmol L−1 Ringer's lactate has an osmolarity of 273 mOsm L−1 and a pH of 6.5. The lactate is metabolized into bicarbonate by the liver, which can help correct metabolic acidosis. Ringer's lactate solution alkalinizes via its consumption in the citric acid cycle, the generation of a molecule of carbon dioxide which is then excreted by the lungs. They increase the strong ion difference in solution, leading to proton consumption and an overall alkalinizing effect.

The diagnosis of intestinal obstruction in the newborn; a review of the literature with a report of eight additional cases.

Because the clinical appearance of newborn infants having intestinal obstruction is disarmingly normal, vomiting is reason for immediate search for the cause. To this end the character of stools and meconium that are passed should be carefully observed, lest valuable time elapse before correct diagnosis is made. In three cases of volvulus observed by the authors, there was moderate to pronounced distention of the abdomen at birth-a sign which may be helpful in diagnosis. Roentgenograms are the most helpful diagnostic aid. Since the roentgenographic appearance of the normal infant abdomen differs from that of the adult, interpretations should be made with that in mind. In this connection the absence of gas shadows is significant. Although there are dangers in the use of barium in infants, early diagnosis is so important that use of the substance is justifiable if it will help in correct appraisal. The treatment is always surgical, and the procedure of choice is primary anastomosis. Proper preoperative and postoperative care and treatment, including maintenance of fluid and electrolyte balance and blood volume, are of great importance.

Anion gap

Sample calculations Given the following data from a patient with severe hypoalbuminemia suffering from postoperative multiple organ failure, calculate the anion gap and the albumin-corrected anion gap. Data: [Na+] = 137 mEq/L; [Cl−] = 102 mEq/L; [HCO] = 24 mEq/L; [Normal Albumin] = 4.4 g/dL; [Observed Albumin] = 0.6 g/dL. Calculations: Anion Gap = [Na+] - ([Cl−] + [HCO]) = 137 - (102 + 24) = 11 mEq/L. Albumin-Corrected Anion Gap = Anion Gap + 2.5 x ([Normal Albumin] - [Observed Albumin]) = 11 + 2.5 x (4.4 - 0.6) = 20.5 mEq/L. In this example, the albumin-corrected anion gap reveals the presence of a significant quantity of unmeasured anions. See also Osmol gap Delta ratio References External links Clinical Physiology of Acid-Base and Electrolyte Disorders Anion Gap Calculator (includes a correction for the albumin concentration) Metabolic acidosis by Merck More information about the Figge-Jabor-Kazda-Fencl equation

[Acute pancreatitis in pregnancy].

This paper describes a case of acute pancreatitis occurring in a patient immediately after delivery and in primigravida. The patient had a family case history of dyslipidemia (Type IV). The pregnancy had been complicated by preeclampsia treated at home with nifedipine tablets (one tablet three times a day) with good results on pressure values; lipidic values were high despite dietary measures taken. The baby at birth weighed 3830 g after physiologic labour and a natural delivery. Acute pancreatitis was diagnosed after observation of epigastralgia with irradiation on the left shoulder, vomiting, symptoms of acute abdomen such as sweating, increased pulse rate, hypotension, abdominal pain on palpation, and absence of peristalsis. An analysis of the blood showed high levels of amylase and hyperglycemia, an increase in XDP, and leucocytosis. Instrumental tests such as pancreatic echography revealed an increase in pancreatic volume, uneven structure of the parenchyma and higher levels of liquid in the peritoneum. The patient was moved to intensive-care, a nasal gastric probe inserted, hydroelectrolytic treatment was begun, vital functions monitored, pain kept under control by medical therapy, and antibiotics administered. Subsequent tests showed an improvement in the parameters of pancreatic functions (amylase, lipase, calcium hematic) and their gradual return to normal values. The computerized tomography of abdomen additionally revealed the presence of pancreatic pseudo-cysts and effusion of peritoneal liquid near the right kidney. The patient was discharged after two weeks in the surgical ward. There are many caused of acute abdomen during and immediately after pregnancy, and one of these is acute pancreatitis, though rare (occurring between 1:3800 and 11.467 according to Rabkin).(ABSTRACT TRUNCATED AT 250 WORDS)

Transient symptomatic hyperglycaemia secondary to inhaled fluticasone propionate in a young child.

Inhaled corticosteroids (ICSs) are currently used to prevent and treat asthma and recurrent wheezing attacks in children. Fluticasone propionate (FP) is one of the most commonly prescribed ICSs because it is considered effective and well tolerated. A male infant of approximately 1 year of age, who was born to parents without relevant clinical problems or family histories including diabetes, was brought to our attention for recurrent wheezing. When he was approximately 2 years old, a regular daily inhaled treatment with FP given using a spacer was prescribed. With this therapy, the child obtained good control of his symptoms with no further recurrences, but after approximately 2 months of treatment he was admitted to the emergency room because he was whining and agitated and exhibited increased diuresis and water intake. Laboratory tests revealed hyperglycaemia (181 mg/dL), mild glycosuria, blood alkalosis (pH 7.49), a bicarbonate level of 31 mmol/L, a pCO2 level of 39 mmHg, a serum sodium level of 135 mEq/L and a serum potassium level of 3.5 mEq/L. The parents confirmed that the recommended dose of FP had been administered with no increase in the amount of drug. The child was immediately treated with endovenous infusion of physiological saline for 24 h, and his glycaemic levels as well as venous blood gas analysis returned to normal, with an absence of glucose in the urine. Oral glucose tolerance test results and glycated haemoglobin levels were normal. Monitoring of blood glucose levels before and after meals for three consecutive days did not reveal any further increase above normal levels. He was discharged with a diagnosis of transient symptomatic hyperglycaemia during ICS therapy and the suggestion to replace his inhaled FP therapy with oral montelukast. Montelukast was continued for 6 months; during this time, the child did not present any other hyperglycaemia episodes. Although there is no evidence of causation, this case report represents an interesting and unusual description of paediatric transient symptomatic hyperglycaemia after treatment with inhaled FP and highlights the importance of considering this potential adverse event and the necessity of informing parents of the possible clinically relevant risks associated with this drug.

[Infant esophageal pH monitoring (author's transl)].

The authors expound their experience of the infant esophageal pH monitoring from a 100 cases statistic. The digestive radiography is necessary for the vomiting infants but the efficiency of radiology is inadequate to diagnose the reflux and particularly to give a sufficient assessment of its intensity. The esophageal pH monitoring performed during a period of 3 hours is a tremendous learning experience; is allows the clinician to take mild reflux and severe reflux into account; performed in several positions, it shows interesting variations that we can turn to account by giving the therapeutic advices. That test is innocuous, easy, little costly, easily repeated; it must have its place beside other investigations and make us advance in the knowledge of a so often found disorder development.

Arterial blood gas test

Guidelines A 1 mmHg change in PaCO2 above or below 40 mmHg results in 0.008 unit change in pH in the opposite direction. The PaCO2 will decrease by about 1 mmHg for every 1 mEq/L reduction in [] below 24 mEq/L A change in [] of 10 mEq/L will result in a change in pH of approximately 0.15 pH units in the same direction. Assess relation of pCO2 with pH: If pCO2 & pH are moving in opposite directions i.e., pCO2 ↑ when pH is <7.4 or pCO2 ↓ when pH > 7.4, it is a primary respiratory disorder. If pCO2 & pH are moving in same direction i.e., pCO2 ↑when pH is >7.4 or pCO2 ↓ when pH < 7.4, it is a primary metabolic disorder. Parameters and reference ranges These are typical reference ranges, although various analysers and laboratories may employ different ranges.

[Congenital chloride diarrhea mimicking meconium ileus in newborn].

Congenital chloride diarrhoea is a rare autosomal recessive disease and the diagnosis is frequently delayed. The disease is most common in Saudi Arabia and Kuwait 1:3200-13 000 births, Finland - 1:30 000-40 000, and in Poland - 1:200 000. Congenital chloride diarrhoea begins in fetal life. The main clinical sign is watery diarrhea that in utero leads to dilated bowel loops, polyhydramnios and often premature birth. Newborns have distended abdomens, absence of meconium, dilated bowel loops in ultrasonography and watery diarrhea which can sometimes be mistaken for urine. The absence of meconium and the distended abdomen suggest meconium ileus or Hirschsprung disease and can lead to unnecessary surgical intervention. The article is a report on a 3-months old boy with the history of dilated bowel loops in prenatal ultrasonograhy, low birth weight and abdominal distention. Because of the suspicion of mechanical bowel obstruction he had laparotomy on the second day of his life. Mechanical obstruction was excluded and enterostomy was performed. Hyponatremia, hypokaliemia and metabolic alkalosis were found in laboratory tests. The electrolyte disturbances were corrected and enterostomy was closed after six weeks. The final diagnosis of congenital chloride diarrhea was established two months later, when the patient was admitted to hospital again with severe watery diarrhea, metabolic alkalosis, hypochloraemia and hypokalemia. The stool chloride concentration was >90 mmol/L. Water and electrolyte deficits had been corrected. The patient was discharged home with supplementation of sodium, potassium and chloride. His follow-up was uneventful. He remains under the care of the pediatric clinic.

Anion gap

The concentrations are expressed in units of milliequivalents/liter (mEq/L) or in millimoles/litre (mmol/L). With potassium The anion gap is calculated by subtracting the serum concentrations of chloride and bicarbonate (anions) from the concentrations of sodium and potassium (cations): = ([Na+] + [K+]) − ([Cl−] + [HCO]) = 20 mEq/L Without potassium Because potassium concentrations are very low, they usually have little effect on the calculated gap. Therefore, omission of potassium has become widely accepted. This leaves the following equation: = [Na+] - ([Cl−] + [HCO]) Normal AG = 8-16 mEq/L Expressed in words, the equation is: Anion Gap = Sodium - (Chloride + Bicarbonate) which is logically equivalent to: Anion Gap = (the most prevalent cation) minus (the sum of the most prevalent anions) (Bicarbonate may also be referred to as "total CO2" or "carbon dioxide".)

[Gastroesophageal reflux in infants: ultrasonographic reading of pHmetry].

pH monitoring of the distal esophagus has proved both sensitive and specific in the detection of reflux but has several limitations due to changes over time in esophageal pH and possibility of alkaline reflux. Simultaneous ultrasonographic monitoring can be helpful when interpreting the results. One thousand infants (80% under 1 year of age) were examined: 500 suffered from vomiting (310 patients), life-threatening events (65 patients) or repeated respiratory diseases (125 patients). Five hundred infants were controls (320 asymptomatic and 180 sibs of patients with SIDS). pHmonitoring and ultrasonography were performed before and after ingestion of milk by vomiting patients and after administration of orange juice in the other symptomatic patients. Control patients were given milk when asymptomatic or orange juice when they belonged to a SIDS sibship. Ultrasonography permitted to interpret the different phases of the pH curves according to the age of patients, the meals and their nature, the events associated with temporary increase in abdominal pressure, the gravity. pH monitoring was able to recognize 1589 acid reflux but failed to recognize 2091 reflux episodes. While pHmonitoring is helpful to demonstrate a relationship between the reflux and such events as apnea, bradycardia, cough, ultrasonography defines a risk based on specificity of reflux and laryngeal or esophageal dysfunction.

[Electrolyte abnormalities and metabolic acidosis in two Duchenne muscular dystrophy patients with advanced congestive heart failure].

We experienced two Duchenne muscular dystrophy patients with advanced congestive heart failure, who showed abrupt severe hyponatremia, hyperkalemia and metabolic acidosis. Two patients received respiratory management, parenteral nutrition, and drugs including angiotensin converting enzyme inhibitors (ACEI). The patient 1 who was 19 years old showed abdominal pain, hematuria, diarrhea and disorientation. Laboratory findings were as follows; Na 120 mEq/L, K 7.3 mEq/L, BUN > 140 mg/dl (scale over), ACTH 20.2 pg/ml, cortisol 25 micrograms/dl, renin 40.7 ng/ml/hr and aldosterone 203 ng/dl. Arterial blood gas analysis (ABG) showed metabolic acidosis (pH 7.232). Combination therapy with hydrocortisone, glucose-insulin therapy (GIT) and NaHCO3 successfully rescued this patient. The patient 2 (28 years of age) was admitted to our hospital because of congestive heart failure. Laboratory findings were as follows; Na 129 mEq/L, K 5.5 mEq/L, BUN 60 mg/dl, cortisol 21 micrograms/dl, renin 36 ng/ml/hr and aldosterone 47 ng/dl. He complained abdominal discomforts from the next day of admission. Ten days after the admission Na, K and BUN were 111 mEq/L, 6.2 mEq/L and 154 mg/dl, respectively. ABG showed compensated metabolic acidosis. He fell into shock during GIT therapy. Laboratory findings at that time were as follows; Na 108 mEq/L, K 3.2 mEq/L, ACTH 77.6 pg/ml, cortisol 24 micrograms/dl, renin 58 ng/ml/hr and aldosterone 24 ng/dl. Although hydrocortisone was introduced, he could not recover and died. There are some reports about life-threatening electrolyte abnormalities and metabolic acidosis in the patients receiving ACEI. These phenomena were more frequent in patients with renal dysfunction and/or congestive heart failure. Hyponatremia, hypovolemia, combination therapy with nonsteroidal anti-inflammatory drugs (NSAID) and/or potassium sparing diuretics were reported as risk factors. We could not prove the correlation between the acute changes in our cases and ACEI. However ACEI is suspicious, because many of these risk factors were observed in our cases. Aldosterone was extremely elevated in the patient 1 when potassium was severely elevated. On the other hand, the patient 2 showed lower aldosterone level after correction of potassium than that on admission. Potassium is regarded as a major secretion factor of aldosterone for patients receiving ACEI. The fact the patient 2 fell into shock during GIT, tells us that we should use steroid simultaneously when we try to correct potassium quickly in severe cases, because acute reduction of potassium may decrease aldosterone. Today, ACEI is a common drug for CHF, so we should pay attentions that ACEI could cause such acute changes. To prevent such acute changes, excessive restriction of water and sodium intake should be avoided. If possible, NSAID and potassium sparing diuretics also should be avoided. Steroid therapy must be introduced rapidly when needed.

Studies on diarrhea in neonatal calves. 3. Acid-base and serum electrolyte values in normal calves from birth to ten days of age.

A detailed clinical examination was conducted and blood samples were collected from a total of 151 normal calves as soon as possible after birth and at two to three day intervals until the calves were ten days old. The mean venous pH values for calves from birth to ten days of age was 7.38 +/- 0.05. The mean serum sodium, potassium, magnesium, inorganic phosphate, calcium and chloride ion concentrations in normal calves from birth to ten days of age were 148 +/- 13, 5.4 +/- 0.8, 2.1 +/- 0.4, 4.3 +/- 0.8, 5.6 +/- 0.5, 95 +/-5, mEq/litre respectively. The mean serum osmolality in normal calves from birth to ten days of age was 280 +/- 12 mOsm/litre.

Biochemistry_Lippinco

Case 8: No Bowel Movement Patient Presentation: DW is a 48-hour-old female who has not yet had a bowel movement. Focused History: DW is the full-term product of a normal pregnancy and delivery. She appeared normal at birth. DW is the first child of parents of Northern European ethnicity. The parents are both in good health, and their family histories are unremarkable. Pertinent Findings: DW has a distended abdomen. She recently vomited small amounts of bilious (green-colored) material. Diagnosis: Meconium ileus (obstruction of the ileum by meconium, the first stool produced by newborns) was confirmed by abdominal x-rays. About 98% of full-term newborns with meconium ileus have cystic fibrosis (CF). Diagnosis of CF was subsequently confirmed with a chloride sweat test. Treatment: The ileus was successfully treated nonsurgically. For management of the CF, the family was referred to the CF center at the regional children’s hospital.

Base excess

Base excess (or deficit) is one of several values typically reported with arterial blood gas analysis that is derived from other measured data. The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958. Estimation Base excess can be estimated from the bicarbonate concentration ([HCO3−]) and pH by the equation: with units of mEq/L. The same can be alternatively expressed as Calculations are based on the Henderson-Hasselbalch equation: Ultimately the end result is: Interpretation Base excess beyond the reference range indicates metabolic alkalosis if too high (more than +2 mEq/L) metabolic acidosis if too low (less than −2 mEq/L)

Clinical presentation of hypernatremic dehydration in exclusively breast-fed neonates.

To identify the clinical presentation of dehydration related to failure of lactation in exclusively breast-fed term infants. A prospective study was performed between January 2000 and June 2003 in Al Qassimi Hospital in the Emirate of Sharjah. Enrollment criteria included term neonates whose birth weight of > 2000 g with no underlying organic illness causing poor feeding admitted for clinical manifestations of dehydration with weight loss of > 10% during the first 2 weeks of life. The control group, a non-randomized sample included healthy full term neonates, seen in Sharjah maternal and child health care center at 4-7 days old for their routine Guthrie screening test. For each dehydrated neonate we took two neonates as controls. Mother's age, parity, length of pregnancy, any pathologic conditions, breastfeeding history and her level of knowledge of lactation was recorded. Neonatal information included mode of delivery, percentage of weight loss, clinical examination, and stool and urine output the previous day. Data was analyzed with Student 't' test and chi-square test. Out of 17208 live births, 29 neonates between the ages of 2-13 days were admitted with weight loss of between 12 and 29% (dehydrated group). 27 patients had hypernatremic dehydration with serum sodium level ranging from 150 to 195 mmol/l. Mean age of admission was 4.9 days. Reasons for admission were: signs of dehydration (55%); hyperthermia (55%); hypoglycemia (27%) and jaundice (59%). The control group included 58 healthy neonates. Their birth weight and age were comparable to those in the dehydrated group. In comparison with the control group, delivery by cesarean section (P< 0.0001), lower level of maternal breastfeeding knowledge (P=0.03), transient inadequate breast milk quantity (P=0.005) and nipple anomalies (P=0.001) was significantly more common in the dehydrated group. Fewer voidings of urine (< 6 times /day) and stool (< 3 times/day) in the previous 24 hours before admission was more frequently observed in the dehydrated group (P < 0.0001). Low level of maternal knowledge in lactation, cesarean section and failure of early postnatal follow up was associated with the neonatal dehydration. Decreased urine and stool frequency might be considered as a warning for failure of lactation.

Changes in oxygen content and acid-base balance in arterial and portal blood in response to the dietary electrolyte balance in pigs during a 9-h period after a meal.

The effect of two dietary electrolyte balance (dEB, Na+ + K+ - Cl-) levels on arterial and portal blood oxygen content, blood pH, and acid-base status in pigs was studied during a 9-h period after a meal, using a crossover experimental design. The dEB levels were established by changing the Cl- level in the diets. Four pigs with a mean weight of 45 kg were surgically fitted with catheters in the carotid artery and portal vein. Two dEB levels (-100 and 200 mEq/kg) were evaluated in two periods of 1 wk each. Feed was given at 2.6 times the maintenance requirement for energy in two meals per day. Water was freely available. Blood samples were taken at 0, 0.5, 1, 1.5, 2, 3, 4, 6, and 9 h after feeding. Blood hemoglobin; O2 pressure; O2 saturation; O2 content; pH; PCO2; HCO3-; base excess; and Na+, K+, and Cl- contents were measured. Oxygen contents in arterial and portal blood were lower (P < 0.008) in the -100 mEq/kg group (5.78 and 4.82 mmol/L respectively) compared to the 200 mEq/kg group (6.18 and 4.99 mmol/L respectively). This was related to the lower hemoglobin content in the blood of animals in the -100 mEq/kg group. Arterial and portal blood pH were lower (P < 0.003) at -100 mEq/kg (7.46 and 7.37) than at 200 mEq/kg (7.49 and 7.43). The difference in blood pH between the two groups was sustained throughout the sampling period. The average values of arterial and portal blood for base excess and HCO3- content were higher (P < 0.001) at high dEB (6.96 and 31.0 mmol/L, respectively, for -100 mEq/kg and 12.54 and 35.9 mmol/ L, respectively, for 200 mEq/kg). The Na+ concentration in the blood was increased and K+ and Cl- concentrations were decreased (P < 0.02) by increasing dEB from -100 mEq/kg to 200 mEq/kg. Blood electrolyte balance level was higher (P < 0.001) in the 200 mEq/kg dEB group than in the -100 mEq/kg dEB group. In conclusion, dEB changed blood oxygen content and pH, and influenced the acid-base buffer system in pigs. Also, within each group, pigs maintained a relatively constant blood pH level during the 9-h period after feeding.

[Evaluation of an insufflatabe abdominal girdle in shortening the second stage of labor].

A prospective study to evaluate the role of the insufflatable abdominal girdle (IAG) in shortening the second stage of labor was carried out in 160 consecutive full-term normal primiparas with vertex presentation. The parturients were randomized in order into 2 groups: the study group (using IAG) and the control group, each containing 80 cases. The average duration of second stage of labor was 40'23" for the cases of the study group and 59'59" for the controls. The difference was statistically significant (P less than 0.01). The average duration between the appearance of fetal head at the vulva to the complete birth of the baby was 11'56" and 20'56" respectively and again the difference was highly significant (P less than 0.01). Vacuum exteractor necessary for the termination of labor was performed in 15 cases of the controls and only 5 cases of the study group. There was no difference of incidence of abnormal fetal heart rate and appearance of meconium-stained aminotic fluid between two groups. The average Apgar score at 1 minute after birth was 9.78 for the study group and 9.88 for the control group (P greater than 0.005). Results of blood gas analysis of umbilical artery and vein immediately after birth, including pH, PO2, PC2 and BE, were all within normal ranges. Maternal blood pressure, pulse, respiratory rate and blood gas analysis were monitored during the second stage of labor and no significant difference was observed between two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular glycoside-like intoxication following ingestion of Thevetia nereifolia/peruviana seeds: a case report.

Some plants contain glycoside compounds which determine cardiovascular symptoms similar to those observed after acute toxic digoxin administration. The present case report involves a patient who showed important cardiovascular symptoms following the ingestion of Thevetia nereifolia/peruviana seeds. About 30 min after ingestion, a 65-year-old man presented with dizziness, giddiness, numbness and a burning sensation, diarrhea, sweating, vomiting and ECG changes. At the time of admission he presented with tremors; his body temperature was 37 degrees C, and blood analysis gave the following results: K 5.6 mEq/l, myoglobin 176 IU, troponin T 0.10 ng/ml, PO2 69 mmHg, PCO2 37.4 mmHg, pH 7.33, HCO3- 19.9 mEq/l, hemoglobin 14.8 g/dl, saturation 92.5%. Echocardiography showed a left ventricle with normal global and segmentary contractility. The following days, the patient showed a reduction, until total resolution, of the atrioventricular block and of the alterations of the ST segment. The ectopic beats also resolved; K value before discharge was 4.4 mEq/l. On the third day, the serum levels of digoxin were 0.15 ng/ml. This case report is important because it describes all the cardiovascular and non-cardiovascular signs of glycoside toxicity in an adult patient who accidentally swallowed only two seeds (non-fatal dose) of Thevetia.

InternalMed_Harrison

Moderatec,d <4 months (<5 kg) 200–400 mL of ORS 4–11 months (5–<8 kg) 400–600 mL of ORS 12–23 months (8–<11 kg) 600–800 mL of ORS 2–4 years (11–<16 kg) 800–1200 mL of ORS 5–14 years (16–<30 kg) 1200–2200 mL of ORS ≥15 years (≥30 kg) 2200–4000 mL of ORS All ages and weights Undertake IV fluid replacement with Ringer’s lactate (or, if not available, normal saline). Give 100 mL/kg in the first 3-h period (or the first 6-h period for children <12 months old); start rapidly, then slow down. Give a total of 200 mL/ kg in the first 24 h. Continue until the patient is awake, can ingest ORS, and no longer has a weak pulse. aAdapted from World Health Organization: First steps for managing an outbreak of acute diarrhoea. Global Task Force on Cholera Control, 2009 (www.who.int/topics/cholera). bContinue normal feeding during treatment. cReassess regularly; monitor stool and vomit output. dVolumes of ORS listed should be given within the first 4 h. Abbreviation: ORS, oral rehydration solution.

A challenging coexistence of central diabetes insipidus and cerebral salt wasting syndrome: a case report.

Combined central diabetes insipidus and cerebral salt wasting syndrome is a rare clinical finding. However, when this happens, mortality is high due to delayed diagnosis and/or inadequate treatment. A 42-year-old white man was referred to neurosurgery due to a non-functional pituitary macroadenoma. He underwent a partial resection of the tumor on July 2, 2015. On the day following surgery he presented polyuria with sodium 149 mEq/L, plasma osmolality 301 mOsm/kg, and urine osmolality 293 mOsm/kg. He started nasal desmopressin 0.05 mg/day with good response. He was already on dexamethasone 4 mg and levothyroxine 75 mcg due to hypopituitarism after surgery. On July 9 he became confused. Cerebral computed tomography was performed with no significant changes. His natremia dropped to 128 mEq/L with development of polyuria despite maintenance of desmopressin dose. His hemoglobin and hematocrit rose from 9.1 g/L to 11.6 g/L and 27.5 to 32.5, respectively. His thyroid function was normal and he was on hydrocortisone 30 mg/day. At 12 p.m. 150 mg/hydrocortisone infusion was initiated, but sodium did not increase. Plasma and urine osmolality were 264 mOsm/kg and 679 mOsm/kg, respectively. At 4 p.m. hydrocortisone was increased and hypertonic saline replacement started. Two hours later he was dehydrated with polyuria and vomiting, and natremia of 124 mEq/L. Hyponatremia was very resistant to treatment despite hypertonic saline replacement, hence desmopressin was suspended. The following day, urine spot analysis showed that natriuresis was 63 mEq/L with serum sodium 132 mEq/L. This was interpreted as a cerebral salt wasting syndrome and control was achieved with aggressive hypertonic saline replacements and fludrocortisone 0.1 mg/three times a day. We present a rare case of a patient with diabetes insipidus and cerebral salt wasting syndrome, who was successfully treated. Hyponatremia in a patient with diabetes insipidus may erroneously be interpreted as inadequate diabetes insipidus control or as syndrome of inappropriate antidiuretic hormone secretion, leading to therapeutic errors. Thus, all clinical and analytical data should be evaluated together for early and correct diagnosis.

[Oral rehydration solutions with 60 or 90 nmol/L of sodium for infants with acute diarrhea in accord with their nutritional status].

A total of 186 infants suffering from dehydration due to acute diarrhea were studied and divided into two groups: 84 children were placed in group A and received the oral rehydration solution (ORS) recommended by the World Health Organization (WHO), know as ORS-90 and those placed in group B were given an ORS with 60 and 90 mmol/L of sodium and glucose, respectively, with an osmolality of 240 mOsm/kg (ORS-60). Seven patients from group A (8.3%) and two from group B (2.5%) could not be orally rehydrated and required intravenous rehydration. The children were divided according to their weight for their age into eutrophics, grade I malnutrition (10 to 25% deficit), grade II (26 to 40% deficit) and grade III (more than 40% deficit). In those patients who evolved favorably, the average rehydration time was 4.5 to 5.3 hours, independently from their nutritional state. In the same way, no important variations were seen in the average sodium and potassium serum levels once the dehydration was corrected, in either of the groups. Yet, both groups showed a persistence in hypokalemia and hyperkalemia seen when admitted, once the dehydration was corrected, demonstrating that the short time needed for the correction of the dehydration was insufficient to completely corrected the changes in serum potassium. Closer studies must be conducted on the hydric balance to adequately demonstrate if the new ORS-60 induces lesser losses through vomiting and feces when compared to the ORS-90 recommended by the WHO.

Periodic paralysis: rare presenting symptom of thyrotoxicosis.

Paralysis due to hypokalemia results from an acute shift of potassium into cells or excessive potassium deficit. In the absence of potassium deficit, it is observed in Familial Hypokalemic Periodic Paralysis and in Thyrotoxic Hypokalemic Periodic Paralysis (TPP). This report describes the initial presentation of hyperthyroidism as sudden quadriplegia associated with hypokalemia. A healthy 25-year-old Puerto Rican policeman came to the emergency room with sudden paralysis in the four extremities of five hours evolution. He woke up in the morning and could not get up. The day before admission his legs felt weak, and it was hard to get out of bed. He arrived home at 7:00 PM, ate pasta and vegetables, and went to sleep at 10:00 PM. He had no diarrhea or weight loss, no history of medications or illicit drugs. He has a cousin and an aunt with the diagnosis of hypo-thyroidism. The admission temperature was 36.0 degrees C, pulse 96 per minute, respiratory rate 18 per minute, blood pressure 160/70 mmHg. He was alert and oriented as to time, place and person. He could talk properly and was in no respiratory distress. He had no exophtalmos or lid lag. The thyroid was not enlarged or tender. No pseudoclubbing or pretibial edema was found. There was flaccid paralysis of all extremities, 0/5 legs and 1/5 arms. Deep tendon reflexes could not be elicited. The cranial nerves and sensory examination were normal. The hemogram was within normal limits as were the renal and liver functions. Serum sodium was 140 mEq/L, potassium 1.48 mEq/L, phosphorus 1.4 mEq/L. A random glucose was 155 mg/dl and the arterial Ph was 7.41. The urine potassium was 7.04 mEq/L, sodium 60.8 mg/dl. TSH levelwas < 0.03 ug/d], TUP 50.69% (24-40%), T4 17.6 ug/dl (4.7-11.4 ug/dl) Free T4 Index 28.23. He was managed with intravenous potassium chloride, 80 mEq in a period of seven hours with cardiac monitor. The serum potassium level, after the infusion was completed, was 6.70 mEq/L. No cardiac arrhythmia was documented. Muscle strength recovery was gradual and it was complete 4 hours after the infusion was initiated. The next day the potassium level was within normal limits but a wide pulse pressure and tachycardia still persisted.

Meconium ileus in newborns with cystic fibrosis - results of treatment in the group of patients operated on in the years 2000-2014.

Evaluation of diagnostic and treatment procedures in children with cystic fibrosis (CF) operated on because of meconium ileus (MI). The authors retrospectively reviewed the documentation of 10 CF newborn patients operated on in the years 2000-2014 because of MI. In prenatal ultrasound (US) examinations, suspicion of bowel abnormalities was raised in 2 cases, even though all the 10 mothers had a minimum of 3 US examinations during pregnancy. The mean gestational age of the newborns was 39.2 weeks - 36-41 weeks), their mean birth weight 3472g (2560-4550 g). Family history of CF was positive in two patients. Genetic testing was performed in all the children operated on. In all the children operated on, mutations in both alleles of the CFTR gene were found. Five patients were F508del homozygotic, 4 were heterozygotic for this mutation, one had another mutation. Sweat tests were positive in all the children. Abdominal distention was observed in 9 patients, vomiting and retention of gastric contents in 5. In 8 children meconium was not passed at all. 2 children passed a small amount of viscid meconium. Before the operation, rectal saline washouts were done in 5 newborns. Five patients were operated on during the first day of life, four on the second day and one on the third day of life. Intra-operatively a simple form of MI was diagnosed in 8 cases, a complicated form in 2 cases. In patients with the simple form of MI, a Bishop-Koop stoma was created after the evacuation of meconium. Two of these children needed a resection of some centimetres of dilated terminal ileum with doubtful viability. In newborns with the complicated form of MI, the treatment was individualized, always with stoma formation. The time of postoperative meconium evacuation through enterostomy ranged from 6 to 15 days. Enteral feeding was started on average on the 9th day postoperatively. The mean hospital stay was 22.9 days. In 8 children the stoma was taken out at the mean age of 19.4 months, in one patient the stoma closed spontaneously. No disturbances in electrolyte balance or excessive fluid loss, nor any body weight deficits connected with the stoma were observed. There were no complications during stoma closure. All the patients are alive. The time of observation ranges from 7 to 146 months (average 95 months). All the patients currently present respiratory symptoms, have pancreatic insufficiency and need pancreatic enzyme supplementation. Seven do not, however, have body weight and height deficits. All the children with weight and height deficits have abnormal liver function tests. During observation two patients had MI equivalent symptoms, which was resolved by conservative treatment. 1. In every case of intra-operative diagnosis of MI, it is necessary to perform genetic testing and sweat tests to confirm or exclude CF. 2. Mechanical intra-operative decompression of the bowel from inspissated meconium with a temporary stoma, which makes the continuation of bowel decompression possible in the postoperative period, is an effective treatment in children with MI. 3. The Bishop-Koop stoma, permitting the passage through the whole gastrointestinal tract, is a safe option. In our material, no complications of this stoma, such as stoma care problems or dyselectrolithemia were observed. 4. The decision of stoma closure in children with MI and CF should be delayed until the moment of introducing a broadened diet and should be undertaken together with a pediatrician who is a specialist in CF therapy. .

Metabolic acidosis

Diagnostic approach and causes Metabolic Acidosis is defined as a reduced serum pH, and an abnormal serum bicarbonate concentration of <22 mEq/L, below the normal range of 22 to 29 mEq/L. However, if a patient has other coexisting acid-base disorders, the pH level may be low, normal or high in the setting of metabolic acidosis. In the absence of chronic respiratory alkalosis, metabolic acidosis can be clinically diagnosed by measuring serum bicarbonate levels in the blood, which is generally a standard component of blood panels. Imperatively, when weighing a metabolic acidosis diagnosis, the change in serum bicarbonate levels over time should be considered; if baseline bicarbonate results are unknown, a single set of values may be misinterpreted. Causes Generally, metabolic acidosis occurs when the body produces too much acid (e.g., lactic acidosis, see below section), there is a loss of bicarbonate from the blood, or when the kidneys are not removing enough acid from the body.

[Acute abdomen in pediatric roentgenology (author's transl)].

In vue of the successes of modern surgery, correct roentgenology in acute abdominal conditions of the infant and child is of utmost importance. History is very incomplete in children so that the most crucial question is when and how should X-ray investigation start? The answer is difficult to provide because of the necessity of early surgery which, in addition can be hindered by an unnecessary roentgenography. Often this cannot be repeated because of worsening in the patient's condition. Knowledge of specific pathology and of congenital malformations is necessary. One must be careful in using contrast medium in acute abdomens as it may worsen the situation. Hypertonic solutions can heavily modifie the fluid and electrolyte balance, especially in dehydrated children. Technical aspects deserve attention, for instance for treatment of invagination, or in congenital megacolon. The authors illustrate these problems with a few cases.

Cutaneous manifestations of Strongyloides stercoralis hyperinfection in an HIV-seropositive patient.

A 41-year-old human immunodeficiency virus (HIV)-positive man was hospitalized with complaints of a 4-week history of nausea and vomiting, associated with decreased oral intake, and a 4-day history of frontal headache and fever. His medical history was significant for a gunshot wound to the head 3 years prior, with a residual seizure disorder. He also had two previous hospitalizations, both for culture-negative bacterial meningitis; the first episode occurred 12 months before admission and the second episode occurred 5 months later. At that time, he was found to be positive for serum antibodies against HIV and a CD4+ T-lymphocyte count of 126/mm3. He had no known drug allergies and was not receiving any medication. On admission, the patient was febrile (104.0 degrees F) and hypotensive (blood pressure, 92/40 mm Hg). Pertinent physical examination findings included cachexia with bitemporal wasting, dry mucus membranes, adherent white patches on the oral mucosa, and negative Kernig's and Brudzinski's signs. His laboratory results revealed macrocytic anemia, a decreased serum sodium of 125 mEq/L, and a normal total leukocyte count with a CD4+ T-lymphocyte count < 50/mm3. Lumbar puncture opening pressure was elevated at 160 mm Hg, and cerebrospinal fluid analysis showed an increased white cell count of 97/microL (84% lymphocytes), a decreased glucose level of 26 mg/dL, and a decreased protein level of 42 mg/dL. The patient was started on empiric therapy that included intravenous ampicillin and cefotaxime, oral Bactrim, and clotrimazole lozenges for thrush. Cerebrospinal fluid culture was positive for Escherichia coli, sensitive to cefotaxime. Two days later, the patient developed fine, erythematous, nonblanchable macules primarily on his abdomen, with minimal involvement of his thorax and back. His skin lesions remained unchanged for the next 2 weeks. Repeat lumbar puncture was performed after 14 days of cefotaxime. The cerebrospinal fluid analysis showed an elevated white cell count of 7/microL (100% lymphocytes), a decreased glucose level of 53 mg/dL, and a decreased protein level of 33 mg/dL. The cerebrospinal fluid culture was now positive for Pseudomonas aeruginosa resistant to cefotaxime. The patient was started on imipenem. On day 34 of his admission, the patient became tachypneic with complaints of dyspnea. A chest roentgenogram revealed bilateral patchy infiltrates. He was transferred to the intensive care unit and intubated for hypoxemic respiratory failure (arterial blood gas values on 6 L of oxygen: pH, 7.46; bicarbonate, 23; and oxygen saturation, 37). That evening, the patient was also noted to have diffuse petechiae and purpura in a reticulated pattern over his abdomen (Figure 1A and 1B), most heavily concentrated in the periumbilical region, extending to the axillae and upper thighs. A 3x3-mm punch biopsy from abdominal skin demonstrated Strongyloides stercoralis larvae in the dermis (Figure 2A and 2B). His sputum specimen was teeming with adult S stercoralis worms (Figure 3) and, subsequently, numerous S stercoralis larvae were observed not only from the bronchoalveolar lavage but also from the nasogastric fluid specimen. These findings confirmed the diagnosis of disseminated strongyloidiasis. On hospital day 35, the patient was doing poorly and was started on thiabendazole (1250 mg twice daily for 28 days). Nine days later, ivermectin (4.5 mg once daily for 3 days for 2 courses) was also added. He continued to clinically deteriorate. The patient died 31 days after systemic antihelminthic treatment was initiated.

[Bulimia, induced vomiting, hypochloremic-hypokalemic alkalosis and fetal distress in the 33rd week of pregnancy. Obstetric and anesthesiologic management].

A 39-year-old primigravida was admitted to the hospital in the 33rd week of pregnancy due to fetal retardation and placental insufficiency, malnutrition, decreased cutaneous turgor, and cardiotocographic (CTG) fetal distress. Body weight had increased subnormally through the 29th week of gestation and had since decreased by 2.5 kg. The following laboratory tests were obtained (normal values for pregnant women in parentheses): serum bicarbonate 50.9 (20-24) mmol/l, pH 7.61 (7.4), PCO2 52.4 (31) mmHg, SaO2 89-91 (greater than 95%); serum sodium 125 (137-145), potassium 1.8 (3.6-5.5), chloride 55 (94-111) mmol/l; colloid osmotic pressure 20.7 (19-22) mmHg. A decompensated hypochloremic-hypokalemic acidosis together with hypovolemic, isotonic hyponatremia was diagnosed and bulimic vomiting that had existed for two decades was discovered as the underlying cause. The acute therapy was aimed at normalization of the fluid-electrolyte status, oxygenation, utero-placental perfusion, and placental-fetal O2 transfer and was carried out under close clinical, biochemical, and CTG surveillance. In addition to the basic measures (lateral tilt position, nasal O2 application, isotonic electrolyte solutions, parenteral nutrition), 158 mmol H+, 240 mmol K+, and 414 mmol Na+ ions were administered. This therapy improved the maternal and fetal parameters continuously (Table 3, Fig. 1). Twenty-six hours following the initiation of treatment, a cesarean section was performed after induction of catheter-epidural anesthesia.

Obstentrics_Williams

TABLE 32-3. Umbilical Cord Blood pH and Blood Gas Values in Normal Term Newborns Ramin, 1989a Riley, 1993b Kotaska, 201 Ob Kotaska, 2010e pH 7.28 (0.07) 7.27 (0.069) 7.26 (7.01n-7.39) 7.3 (7.05-7.39) Pco2 (mm Hg) 49.9 (14.2) 50.3(11n.1) 51 (30.9-85.8) 54 (37.5-79.5) HC03 -(mEq/L) 23.1 (2.8) 22.0 (3.6) Base excess (mEq/L) -3.6 (2.8) -2.7 (2.8) pH 7.34 (0.063) 7.31 (7.06-7.44) 7.34 (7.10-7.42) PC02 (mm Hg) 40.7 (7.9) 41 (24.9-70.9) 44 (29.1n-70.2) HC03 -(mEq/L) 21.4 (2.5) Base excess (mEq/L) -2.4 (2) aNewborns of selected women with uncomplicated vaginal deliveries. bNewborns of unselected women with vaginal deliveries. (Data shown as mean (SO). dOata shown as range with 2.5 or 97.5 percentile. eCesarean delivery-labor not stated. From Centers for Disease Control and Prevention, 201n2; Watson, 2006.

Ringer's lactate solution

Ringer's lactate solution is used because the byproducts of lactate metabolism in the liver counteract acidosis, which is a chemical imbalance that occurs with acute fluid loss or kidney failure. The IV dose of Ringer's lactate solution is usually calculated by estimated fluid loss and presumed fluid deficit. For fluid resuscitation the usual rate of administration is 20 to 30 mL/kg body weight/hour. RL is not suitable for maintenance therapy (i.e., maintenance fluids) because the sodium content (130 mEq/L) is considered too low, particularly for children, and the potassium content (4 mEq/L) is too low, in view of electrolyte daily requirement. Moreover, since the lactate is converted into bicarbonate, long-term use will cause patients to become alkalotic. Ringer's lactate and other crystalloids are also used as vehicles for the IV delivery of medications. In a large-volume resuscitation over several hours, LRS maintains a more stable blood pH than normal saline.

[Assessment of the natural history and clinical presentation of acetonemic vomiting].

Ketosis in children may result from physiological adaptation to situations like fasting, fat-rich diet, straining physical activity, as well as from serious endocrine or metabolic disorders. The most frequently diagnosed cause of ketoacidosis are states of acetonemia and acetonuria with vomiting, during airways infections. Assessment of the natural history and clinical presentation of acetonemic vomiting in children. 85 children from 18 months to 12 years of age with acetonemic vomiting were incorporated in this study. Detailed anamnesis, clinical examination, and chosen laboratory parameters were analyzed. In 18% of the children a familial pattern of the disease was observed, 75% of the parents declared that their children had fat-rich meals on a regular basis, in 47% there was a tendency to recurrent respiratory tract. The most frequently observed symptoms were incoercible vomiting with nausea (100%), abdominal pain (87%), headaches (35%) and febrile states (62%). Ketosis triggers were: infections with insufficient fluid and food intake (68%), and child overfeeding with fat-rich products (23%). Observed biochemical disturbances were ketosis (mean J3-hydroxybutyric acid serum concentration--1.03 mmol/l, SD +/- 0.83), acetonuria, hypoglycemia (15%), metabolic acidosis (17%) and dyselectrolytemia (14%). The treatment of the children consisted in intravenous and oral rehydration, managing acid-base and electrolyte disturbances. In some children acetonemic vomiting is recurrent, and thus prophylactic management is im- portant in children who are at risk.


Debut of DM with ketoacidosis. Priority is iv insulin administration and serum therapy. Bicarbonate if pH < 7. Insulin administration should never be delayed.

A 22-year-old female student with no history of pathology or use of medications except anovulatory drugs comes to the emergency department for deterioration of general condition and need to take deep breaths. She reports weight loss in the last 2-3 days, polydipsia, polyuria and nausea. No cough or febrile sensation. Examination: appearance of gravity, blood pressure 100/60 mmHg, deep and rapid breathing (28rpm), level of consciousness preserved, dry mucous membranes. No fever. CBC: blood glucose 420 mg/dL, Na+ 131 mEq/L, K+ normal, pH 7.08, bicarbonate 8 mEq/L and ketonuria (+++) Which answer do you think is more correct?

Debut of type 2 diabetes mellitus, with dyspnea probably due to pneumonia or thromboembolism, since she is taking anovulatory drugs.

It is a diabetic ketoacidosis. It must be treated with intravenous insulin, serum therapy, general measures and search for precipitating cause.

Debut of type 1 diabetes with ketoacidosis. Treat with bicarbonate and after correction of acidosis, add intravenous insulin.

It looks like diabetic ketoacidosis, but it could be alcoholic. BAC should be determined before starting insulin therapy.

Treat with rapid subcutaneous insulin, serum therapy and ask him to drink plenty of fluids.

Diabetic ketoacidosis: evaluation and treatment.

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as information on the importance of medication compliance.

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

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.

Hyperglycemia

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys, which leads to the presence of glucose in the urine. This produces an osmotic diuresis. Signs and symptoms of diabetic ketoacidosis may include: Ketoacidosis Kussmaul hyperventilation (deep, rapid breathing) Confusion or a decreased level of consciousness Dehydration due to glycosuria and osmotic diuresis Increased thirst 'Fruity' smelling breath odor Nausea and vomiting Abdominal pain Impairment of cognitive function, along with increased sadness and anxiety Weight loss

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific "fruity" smell. Onset of symptoms is usually rapid. People without a previous diagnosis of diabetes may develop DKA as the first obvious symptom. DKA happens most often in those with type 1 diabetes but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke and certain medications such as steroids. DKA results from a shortage of insulin; in response, the body switches to burning fatty acids, which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH and ketoacids in either the blood or urine.

Diabetic ketoacidosis

Fluid replacement The amount of fluid replaced depends on the estimated degree of dehydration. If dehydration is so severe as to cause shock (severely decreased blood pressure with insufficient blood supply to the body's organs), or a depressed level of consciousness, rapid infusion of saline (1 liter for adults, 10 ml/kg in repeated doses for children) is recommended to restore circulating volume. Slower rehydration based on calculated water and sodium shortage may be possible if the dehydration is moderate, and again saline is the recommended fluid. Very mild ketoacidosis with no associated vomiting and mild dehydration may be treated with oral rehydration and subcutaneous rather than intravenous insulin under observation for signs of deterioration. Normal saline (0.9% saline) has generally been the fluid of choice. There have been a few small trials looking at balanced fluids with few differences.

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.

Diabulimia

Signs and symptoms A person with diabulimia, especially if not treated early, can suffer negative effects on the body earlier than one who is managing properly. Of diabetics who have a DEB, some intentionally misuse insulin to control weight. This may also involve irregular eating patterns. Suspension of insulin combined with overeating can result in ketoacidosis. Multiple hospitalizations for ketoacidosis or hyperglycemia are cues to screen for an underlying emotional conflict. Short term The short-term symptoms of diabulimia are: Frequent and excessive urination Frequent and excessive thirst Frequent and excessive hunger High blood glucose levels (often over 600 mg/dL or 33 mmol/L) Weakness Fatigue Large amounts of glucose in the urine (glycosuria) Inability to concentrate Electrolyte disturbance Severe ketonuria, and, in DKA, severe ketonemia Low sodium levels

Diabetic ketoacidosis

The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually, potassium is also needed to prevent the development of low blood potassium. Throughout treatment, blood sugar and potassium levels should be regularly checked. Underlying causes for the DKA should be identified. In those with severely low blood pH who are critically ill, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% of type 1 diabetics a year. DKA was first described in 1886, and until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is between <1% and 5%.

[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.

[Opportunities to improve hospital emergency care of patients with diabetic ketoacidosis].

To identify opportunities to improve the care of adult patients with diabetic ketoacidosis in the emergency room. Retrospective observational study of records for 2010 to 2013. Searching for International Classification of Diseases discharge codes 250.1–250.3 we identified patients who met the following 3 criteria: ketonuria of 100 mg/dL or more, diagnosed diabetes or glucose concentration of 250 mg/dL or more, and venous blood pH below 7.30 (or venous bicarbonate concentration less than 18 mEq/L). We reviewed the cases to extract patient and clinical characteristics and time from triage until diagnosis and start of treatment. The findings were compared with recommendations in clinical practice guidelines. We identified 49 episodes of diabetic ketoacidosis (4 mild, 32 moderate, and 13 severe) in 43 patients. The median delay between triage until the first blood test results were available was 142 minutes (range, 59-597 minutes). In 50% of the cases fluid therapy was delayed beyond the time recommended in clinical practice guidelines. Intravenous insulin was also delayed (in 66%) and insuficient intravenous potassium was given in 65%. Sodium bicarbonate was overused (in 50%). Half the patients developed hypokalemia in the hospital. Diagnosis and initiation of treatment were often delayed for patients with diabetic ketoacidosis in our emergency department.

Diabetic ketoacidosis.

A diagnosis of diabetic ketoacidosis requires the patient's plasma glucose concentration to be above 250 mg per dL (although it usually is much higher), the pH level to be less than 7.30, and the bicarbonate level to be 18 mEq per L or less. Beta-hydroxybutyrate is a better measurement of the degree of ketosis than serum ketones. Intravenous insulin and fluid replacement are the mainstays of therapy, with careful monitoring of potassium levels. Phosphorous and magnesium also may need to be replaced. Bicarbonate therapy rarely is needed. Infection, insulin omission, and other problems that may have precipitated ketoacidosis should be treated. Myocardial infarction is a precipitating cause of diabetic ketoacidosis that is especially important to look for in older patients with diabetes. Cerebral edema is a major complication that occurs primarily in children. Education to prevent recurrence should be offered to all patients, including how to manage sick days and when to call a physician.

Diabetic ketoacidosis

Resolution Resolution of DKA is defined as general improvement in the symptoms, such as the ability to tolerate oral nutrition and fluids, normalization of blood acidity (pH>7.3), and absence of ketones in blood (<1 mmol/l) or urine. Once this has been achieved, insulin may be switched to the usual subcutaneously administered regimen, one hour after which the intravenous administration can be discontinued. In people with suspected ketosis-prone type 2 diabetes, determination of antibodies against glutamic acid decarboxylase and islet cells may aid in the decision whether to continue insulin administration long-term (if antibodies are detected), or whether to withdraw insulin and attempt treatment with oral medication as in type 2 diabetes. Generally speaking, routine measurement of C-peptide as a measure of insulin production is not recommended unless there is genuine doubt as to whether someone has type 1 or type 2 diabetes.

Diabetes -- Complications

The most acute complication of DM is diabetic ketoacidosis (DKA), which typically presents in T1DM. This condition is usually either due to inadequate dosing, missed doses, or ongoing infection. [53] In this condition, the lack of insulin means that tissues are unable to obtain glucose from the bloodstream. Compensation for this causes the metabolism of lipids into ketones as a substitute energy source, which causes systemic acidosis, and can be calculated as a high anion-gap metabolic acidosis. The combination of hyperglycemia and ketosis causes diuresis, acidemia, and vomiting leading to dehydration and electrolyte abnormalities, which can be life-threatening. In T2DM, hyperosmolar hyperglycemic syndrome (HHS) is an emergent concern. It presents similarly to DKA with excessive thirst, elevated blood glucose, dry mouth, polyuria, tachypnea, and tachycardia. However, unlike DKA, HHS typically does not present with excessive urinary ketones since insulin still gets produced by pancreatic beta cells. Treatment for DKA or HHS involves insulin administration and aggressive intravenous hydration. Careful management of electrolytes, particularly potassium, is critical in the management of these emergent conditions. [54]

Neurology_Adams

Two syndromes have been defined, mainly in diabetics: (1) hyperglycemia with ketoacidosis and (2) hyperosmolar nonketotic hyperglycemia. In diabetic acidosis, the familiar picture is one of dehydration, fatigue, weakness, headache, abdominal pain, dryness of the mouth, stupor or coma, and Kussmaul type of breathing. Usually the condition has developed over a period of days in a patient known or proven to be diabetic. Often, the patient had failed to take a regular insulin dose. The blood glucose level is found to be more than 400 mg/dL, the pH of the blood less than 7.20, and the bicarbonate less than 10 mEq/L. Ketone bodies and b-hydroxybutyric acid are elevated in the blood and urine, and there is marked glycosuria. The prompt administration of insulin and repletion of intravascular volume correct the clinical and chemical abnormalities over a period of hours.

Diabetes

Diabetic emergencies People with diabetes (usually but not exclusively in type 1 diabetes) may also experience diabetic ketoacidosis (DKA), a metabolic disturbance characterized by nausea, vomiting and abdominal pain, the smell of acetone on the breath, deep breathing known as Kussmaul breathing, and in severe cases a decreased level of consciousness. DKA requires emergency treatment in hospital. A rarer but more dangerous condition is hyperosmolar hyperglycemic state (HHS), which is more common in type 2 diabetes and is mainly the result of dehydration caused by high blood sugars.

Ketosis

Ketosis is a metabolic state characterized by elevated levels of ketone bodies in the blood or urine. Physiologic ketosis is a normal response to low glucose availability, such as low-carbohydrate diets or fasting, that provides an additional energy source for the brain in the form of ketones. In physiologic ketosis, ketones in the blood are elevated above baseline levels, but the body's acid–base homeostasis is maintained. This contrasts with ketoacidosis, an uncontrolled production of ketones that occurs in pathologic states and causes a metabolic acidosis, which is a medical emergency. Ketoacidosis is most commonly the result of complete insulin deficiency in type 1 diabetes or late-stage type 2 diabetes. Ketone levels can be measured in blood, urine or breath and are generally between 0.5 and 3.0 millimolar (mM) in physiologic ketosis, while ketoacidosis may cause blood concentrations greater than 10 mM.

Hyperglycemia -- History and Physical

Symptoms of severe hyperglycemia include polyuria, polydipsia, and weight loss. As the patient's blood glucose increases, neurologic symptoms can develop. The patient may experience lethargy, focal neurologic deficits, or altered mental status. The patient can progress to a comatose state. Patients with diabetic ketoacidosis may present with nausea, vomiting, and abdominal pain in addition to the above symptoms. They also may have a fruity odor to their breath and have rapid shallow respirations, reflecting compensatory hyperventilation for the acidosis. The physical examination can reveal signs of hypovolemia like hypotension, tachycardia, and dry mucous membranes.

A Case of Euglycemic Diabetic Ketoacidosis due to Empagliflozin Use in a Patient with Type 1 Diabetes Mellitus.

Euglycemic diabetic ketoacidosis is characterised by serum blood glucose <250 mg/dl, arterial blood pH <7.35, and the presence of ketones in urine or blood. Here, we present a 36-year female with type-1 diabetes mellitus, a case of euglycemic diabetic ketoacidosis, who was admitted to the emergency unit with nausea, vomiting, and confusion after using empagliflozin, which was added to her treatment one month ago. She was followed up in the intensive care unit for four days. Empagliflozin was discontinued. Intravenous fluids and insulin infusions were given. The patient, whose metabolic acidosis regressed, was discharged with the necessary recommendations and training. Euglycemic diabetic ketoacidosis should be kept in mind as a differential diagnosis in patients with type-1 diabetes and type-2 diabetes presenting with acidosis. Attention should be paid to the patients' medications and whether there are SGLT-2 inhibitors among these drugs. Key Words: Diabetes mellitus, Sodium-glucose co-transporter-2 inhibitors, Euglycemic diabetic ketoacidosis, Empagliflozin.

Diabetic ketoacidosis

A 2004 statement by the European Society for Paediatric Endocrinology and the Lawson Wilkins Pediatric Endocrine Society (for children) uses slightly different cutoffs, where mild DKA is defined by pH 7.20–7.30 (bicarbonate 10–15 mmol/l), moderate DKA by pH 7.1–7.2 (bicarbonate 5–10) and severe DKA by pH<7.1 (bicarbonate below 5). Prevention Attacks of DKA can be prevented in those known to have diabetes to an extent by adherence to "sick day rules"; these are clear-cut instructions to person on how to treat themselves when unwell. Instructions include advice on how much extra insulin to take when sugar levels appear uncontrolled, an easily digestible diet rich in salt and carbohydrates, means to suppress fever and treat infection, and recommendations when to call for medical help. People with diabetes can monitor their own ketone levels when unwell and seek help if they are elevated.

[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy].

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Ketoacidosis

Acetoacetic acid and β-hydroxybutyrate are the most abundant circulating ketone bodies. Ketone bodies are acidic; however, at physiologic concentrations, the body's acid/base buffering system prevents them from changing blood pH. Management Treatment depends on the underlying cause of the ketoacidosis. Diabetic ketoacidosis is resolved with insulin infusion, intravenous fluids, electrolyte replacement and supportive care. Alcoholic ketoacidosis is treated with intravenous dextrose and supportive care and usually does not require insulin. Starvation ketoacidosis can be resolved with intravenous dextrose with attention to electrolyte changes that can occur with refeeding syndrome. Epidemiology Certain populations are predisposed to develop ketoacidosis including people with diabetes, people with a history of prolonged and heavy alcohol use, pregnant women, breastfeeding women, children, and infants.

Diabetes -- History and Physical

During patient history, questions about family history, autoimmune diseases, and insulin-resistant are critical to making the diagnosis of DM. It often presents asymptomatically, but when symptoms develop, patients usually present with polyuria, polydipsia, and weight loss. On physical examination of someone with hyperglycemia, poor skin turgor (from dehydration) and a distinctive fruity odor of their breath (in patients with ketosis) may be present. In the setting of diabetic ketoacidosis (DKA), clinicians may note Kussmaul respirations, fatigue, nausea, and vomiting. Funduscopic examination in a patient with DM may show hemorrhages or exudates on the macula. In frank diabetic retinopathy, retinal venules may appear dilated or occluded. The proliferation of new blood vessels is also a concern for ophthalmologists and can hasten retinal hemorrhages and macular edema, ultimately resulting in blindness. While T1DM and T2DM can present similarly, they can be distinguished based on clinical history and examination. T2DM patients are typically overweight/obese and present with signs of insulin resistance, including acanthosis nigricans, which are hyperpigmented, velvety patches on the skin of the neck, axillary, or inguinal folds. Patients with a longer course of hyperglycemia may have blurry vision, frequent yeast infections, numbness, or neuropathic pain. The clinicians must ask the patient bout any recent skin changes in their feet during each visit. The diabetic foot exam, including the monofilament test, should be a part of the routine physical exam.

Diabetic ketoacidosis

Numerous research studies since the 1950s have focused on the ideal treatment for diabetic ketoacidosis. A significant proportion of these studies have been conducted at the University of Tennessee Health Science Center and Emory University School of Medicine. Treatment options studied have included high- or low-dose intravenous, subcutaneous or intramuscular (e.g. the "Alberti regime") insulin, phosphate supplementation, need for a loading dose of insulin, and appropriateness of using bicarbonate therapy in moderate DKA. Various questions remain unanswered, such as whether bicarbonate administration in severe DKA makes any real difference to the clinical course, and whether an insulin loading dose is needed in adults.

Adult Diabetic Ketoacidosis -- Evaluation

Commonly accepted criteria for diabetic ketoacidosis are blood glucose greater than 250 mg/dl, arterial pH less than 7.3, serum bicarbonate less than 15 mEq/l, and the presence of ketonemia or ketonuria. The normal anion gap is 12 mEq/l. Anion gap greater than 14-15 mEq/l indicates the presence of an increased anion gap metabolic acidosis. [17] Arterial pH may be normal or even raised if other types of metabolic or respiratory alkalosis coexist. Typical examples are vomiting or diuretic use. [18] Blood glucose may be normal or minimally elevated in patients with DKA (<300 mg/dl), where the underlying risk of hypoglycemia preexists, such as in patients with alcohol use disorder or patients receiving insulin or SGLT2 inhibitors.

InternalMed_Harrison

factors, and the management of diabetes during a concurrent illness. During illness or when oral intake is compromised, patients should (1) frequently measure the capillary blood glucose; (2) measure urinary ketones when the serum glucose is >16.5 mmol/L (300 mg/dL); (3) drink fluids to maintain hydration; (4) continue or increase insulin; and (5) seek medical attention if dehydration, persistent vomiting, or uncontrolled hyperglycemia develop. Using these strategies, early DKA can be prevented or detected and treated appropriately on an outpatient basis.

Ketoacidosis

Ketoacidosis is a metabolic state caused by uncontrolled production of ketone bodies that cause a metabolic acidosis. While ketosis refers to any elevation of blood ketones, ketoacidosis is a specific pathologic condition that results in changes in blood pH and requires medical attention. The most common cause of ketoacidosis is diabetic ketoacidosis but can also be caused by alcohol, medications, toxins, and rarely starvation. Signs and symptoms The symptoms of ketoacidosis are variable depending on the underlying cause. The most common symptoms include nausea, vomiting, abdominal pain, and weakness. Breath may also develop the smell of acetone as it is a volatile ketone that can be exhaled. Rapid deep breathing, or Kussmaul breathing, may be present to compensate for the metabolic acidosis. Altered mental status is more common in diabetic than alcoholic ketoacidosis. Causes

Ketoacidosis -- Differential Diagnosis

Hyperosmolar hyperglycemic state (HHS) occurs in the setting of insulin resistance and is more typical of type 2 diabetes. There is sufficient insulin in patients with HHS to suppress lipolysis and production of ketone bodies, but inadequate amounts to prevent the hyperglycemia, dehydration, and hyperosmolality, characteristic of HHS. An illness or event that leads to dehydration will often precipitate the hyperglycemia associated with HHS. The development of HHS is less acute than DKA and may take days to weeks to develop. HHS typically presents with more extreme hyperglycemia and mental status changes compared with DKA. HHS typically presents with normal or small amounts of urine or serum ketones. Plasma glucose values in HHS are typically greater than in DKA and can exceed 1200 mg/dL (66.6 mmol/L). The serum osmolality is elevated greater than 320 mOsm/kg H2O. The serum bicarbonate level is greater than 18 mEq/L (18 mmol/L), and the pH remains greater than 7.3.

Just the Facts: Diagnosis and treatment of diabetic ketoacidosis in the emergency department.

A 21-year-old male with known type 1 diabetes mellitus presented to the emergency department (ED) with two days of vomiting, polyuria, and polydipsia after several days of viral upper respiratory tract infection symptoms. Since his symptom onset, his home capillary blood glucose readings have been higher than usual. On the day of presentation, his glucometer read "high," and he could not tolerate oral fluids. On examination, his pulse was 110 beats/minute, and his respiratory rate was 24 breaths/minute. He was afebrile, and the remaining vital signs were normal. Other than dry mucous membranes, his cardiopulmonary, abdominal, and neurologic exams were unremarkable. Venous blood gas demonstrated a pH of 7.25 mm Hg, pCO2 of 31 mm Hg, HCO3 of 13 mm Hg, anion gap of 18 mmol/L, and laboratory blood glucose of 40 mmol/L, as well as serum ketones measuring "large."

Type 2 diabetes

Type 2 diabetes (T2D), formerly known as adult-onset diabetes, is a form of diabetes that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. Common symptoms include increased thirst, frequent urination, and unexplained weight loss. Symptoms may also include increased hunger, feeling tired, and sores that do not heal. Often symptoms come on slowly. Long-term complications from high blood sugar include heart disease, strokes, diabetic retinopathy which can result in blindness, kidney failure, and poor blood flow in the limbs which may lead to amputations. The sudden onset of hyperosmolar hyperglycemic state may occur; however, ketoacidosis is uncommon. Type 2 diabetes primarily occurs as a result of obesity and lack of exercise. Some people are more genetically at risk than others.

Ketosis

Ketoacidosis Ketoacidosis is a pathological state of uncontrolled production of ketones that results in a metabolic acidosis. Ketoacidosis is most commonly caused by a deficiency of insulin in type 1 diabetes or late stage type 2 diabetes but can also be the result of chronic heavy alcohol use, salicylate poisoning, or isopropyl alcohol ingestion. Ketoacidosis causes significant metabolic derangements and is a life-threatening medical emergency. Ketoacidosis is distinct from physiologic ketosis as it requires failure of the normal regulation of ketone body production. Causes Elevated blood ketone levels are most often caused by accelerated ketone production but may also be caused by consumption of exogenous ketones or precursors.

Intravenous sodium bicarbonate

Commercial production of sodium bicarbonate began between 1791 and 1823. Intravenous medical use began around the 1950s. It is on the World Health Organization's List of Essential Medicines. Sodium bicarbonate is available as a generic medication. Medical uses Intravenous sodium bicarbonate is indicated in the treatment of metabolic acidosis, such as can occur in severe kidney disease, diabetic ketoacidosis, circulatory insufficiency, extracorporeal circulation of blood, in hemolysis requiring alkalinization of the urine to avoid nephrotoxicity of blood pigments, and certain drug intoxications, such as by barbiturate overdose, salicylate poisoning, tricyclic antidepressant overdose or methanol poisoning. In addition, sodium bicarbonate is indicated in severe diarrhea, where large amounts of bicarbonate may be lost. However, overall treatment should also strive to treat the underlying cause of the acidosis, such as giving insulin in case of diabetic ketoacidosis. Dhaka fluid