Kussmaul Breathing Research Articles

A case of a woman with late-pregnancy-onset DKA who had normal glucose tolerance in the first trimester

SummaryDiabetic ketoacidosis (DKA) during pregnancy is a serious complication in both mother and fetus. Most incidences occur during late pregnancy in women with type 1 diabetes mellitus. We report the rare case of a woman with type 1 diabetes mellitus who had normal glucose tolerance during the first trimester but developed DKA during late pregnancy. Although she had initially tested positive for screening of gestational diabetes mellitus during the first trimester, subsequent diagnostic 75-g oral glucose tolerance tests showed normal glucose tolerance. She developed DKA with severe general fatigue in late pregnancy. The patient's general condition improved after treatment for ketoacidosis, and she vaginally delivered a healthy infant at term. The presence of DKA caused by the onset of diabetes should be considered, even if the patient shows normal glucose tolerance during the first trimester.Learning points The presence of DKA caused by the onset of diabetes should be considered, even if the patient shows normal glucose tolerance during the first trimester.Symptoms including severe general fatigue, nausea, and weight loss are important signs to suspect DKA. Findings such as Kussmaul breathing with ketotic odor are also typical.Urinary test, atrial gas analysis, and anion gap are important. If pH shows normal value, calculation of anion gap is important. If the value of anion gap is more than 12, a practitioner should consider the presence of metabolic acidosis.

Management of acute hyperglycemic emergencies: focus on diabetic ketoacidosis.

Management of acute hyperglycemic emergencies: focus on diabetic ketoacidosis.

Precipitating factors, clinical features and outcome of diabetic ketoacidosis in children and adolescents admitted in a tertiary care hospital in Dhaka

Background Information: Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (DM). It is an acute complication of type 1 DM. Objective: This study was designed to identify the precipitating factors, clinical features and immediate outcomes of DKA in children and adolescents. Method: This was a retrospective study which was done in the department of Pediatrics, BIRDEM, from January 2002 to April 2007. Data were collected from the hospital record for all diabetic children below 18 years admitted with DKA. Result: Fourty nine children and adolescents were admitted with DKA. Sixty one percent were known cases and the remaining (39%) were new DM. Majority were female (63%). Most (49%) of the children were between 11- 15 years. Infection was the commonest (49%) precipitating factor followed by insulin omission (24%). Major clinical features were kussmaul breathing (94%) and dehydration (94%).Eighty eight percent patients improved after treatment and mortality was 12%. Conclusion: Infection was the commonest precipitating factor of DKA. Kussmaul breathing and dehydration were the commonest clinical features. Most of the patients improved after treatment.DOI: http://dx.doi.org/10.3329/bjms.v13i1.17429 Bangladesh Journal of Medical Science Vol. 13 No. 01 January2014: 53-57

Type 1 Diabetes Mellitus

1. Justin M. Gregory, MD* 2. Daniel J. Moore, MD, PhD† 3. Jill H. Simmons, MD‡ 1. *Pediatric Endocrinology Clinical Fellow, Ian Burr Division of Pediatric Endocrinology and Diabetes, Vanderbilt University School of Medicine, Nashville, TN. 2. †Assistant Professor of Pediatrics, Assistant Professor of Pathology, Microbiology, and Immunology, Ian Burr Division of Pediatric Endocrinology and Diabetes, Vanderbilt University School of Medicine, Nashville, TN. 3. ‡Assistant Professor of Pediatrics, Ian Burr Division of Pediatric Endocrinology and Diabetes, Vanderbilt University School of Medicine, Nashville, TN. * ADA: : American Diabetes Association DKA: : diabetic ketoacidosis HbA1c: : glycosylated hemoglobin I:C ratio: : insulin-to-carbohydrate ratio IV: : intravenous TDD: : total daily dose T1DM: : type 1 diabetes mellitus T2DM: : type 2 diabetes mellitus 1. All children with type 1 diabetes mellitus (T1DM) should have their blood sugar managed with basal-bolus insulin treatment by either multiple daily injections or an insulin pump. 2. All children with T1DM should have access to a pediatric endocrinologist with a diabetes management team with resources to support patients and families. 3. All children with T1DM should be monitored for symptoms and/or screened for commonly associated conditions such as thyroid and celiac disease. After completing this article, readers should be able to: 1. Recognize the presenting signs and symptoms of type 1 diabetes mellitus (T1DM). 2. Know the key principles of effective diabetes self-management and the diabetes care team’s role in facilitating effective self-management. 3. Know the acute and chronic complications of (T1DM). 4. Identify how different categories of insulin analogues are used in daily insulin regimens. True, it is a fight, but there is pleasure in the struggle. Victory comes to the courageous; and without courage and common sense, success awaits no one. I look upon the diabetic as charioteer and his chariot as drawn by three steeds named Diet, Insulin, and Exercise. It takes skill to drive one horse, intelligence to manage a team of two, but a man must be a very good teamster who can get all three to pull together.EP Joslin, 1933 Type 1 diabetes mellitus (T1DM) is a disorder of glucose homeostasis characterized by autoimmune destruction of the insulin-producing pancreatic β-cell that progressively leads to insulin deficiency and resultant hyperglycemia. If left untreated, insulin deficiency leads to progressive metabolic derangement, with worsening hyperglycemia, ketoacidosis, starvation, and death. In …

Type 1 Diabetes Mellitus

Type 1 Diabetes Mellitus

Hyperglycemic Emergencies in Adults

Hyperglycemic Emergencies in Adults

Madam, why are you so sour?

Madam, why are you so sour?

Delirium in Diabetic Ketoacidosis: A Case Report

A 15-year-old female patient with known type 1 diabetes mellitus was referred because of abdominal pain. On admission, she was alert but dehydrated with marked Kussmaul breathing. Blood glucose was 414 mg/dL (23 mmol/L). Blood gas analysis revealed severe metabolic acidosis (pH: 6.99) with an elevated anion gap (29.8 mmol/L) and an increased base excess (-25.2 mmol/L). At the sixth hour of treatment with intravenous fluids and insulin, the patient became delirious. The delirium persisted despite the normalization of the acidosis and became difficult to manage. Brain imaging studies revealed neither brain edema nor other intracranial pathology. No evidence of intoxication could be found. The patient gradually regained consciousness and was diagnosed as a case of severe diabetic ketoacidosis (DKA) associated with infection. We were unable to find a similar case in the pediatric literature and thought that reporting this unusual case would be a contribution to the literature on DKA in children.Conflict of interest:None declared.

Epidural Pneumatosis and Diffuse Soft Tissue Free Air As a Complication of Diabetic Ketoacidosis

A 23-year-old male with type 1 diabetes presented to the emergency department with insulin nonadherence, vomiting, and sharp neck pain. Laboratory values were consistent with diabetic ketoacidosis (DKA). The physical exam revealed diffuse crepitance around the neck and chest wall. A chest X-ray (Figure 1) showed subcutaneous emphysema (black arrow) and pneumomediastinum (white arrow). A chest computed tomographic scan (Figure 2) revealed extensive pneumomediastinum (thin white arrow) and soft tissue emphysema involving the chest wall, paraspinal musculature, soft tissues (thick black arrow), and epidural pneumatosis (thin black arrow). Rarely reported in the English-language medical literature (1–4), diffuse soft tissue free air associated with DKA is typically benign and likely caused by alveolar rupture from forceful vomiting or Kussmaul respiration (1). Epidural pneumatosis occurs when free air tracks through fascial planes in the brachial plexus, axillary arteries, intercostal nerves, or intervertebral foramina. Our patient's history of emesis raised concern for esophageal perforation, but water-soluble contrast swallow evaluation was normal. The patient fully recovered with conservative management. Figure 1. Chest radiograph showing subcutaneous emphysema (black arrow) and pneumomediastinum (white arrow). Figure 2. Chest computed tomography image showing pneumomediastinum (white arrow), subcutaneous emphysema (thick black arrow), and epidural pneumatosis (thin black arrow).

Diabetic Ketoacidosis Complicated With Previously Unknown Gitelman Syndrome in a Tunisian Child

Gitelman syndrome (GS) is an autosomal recessive disease characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria (1). In the great majority of cases, GS is caused by mutations in the SLC12A3 gene encoding the thiazide-sensitive NaCl cotransporter ( NCCT ), which is specifically expressed in the apical membrane of cells along the distal convoluted tubule (2). A 10-year-old Tunisian male patient was admitted with polyuria, polydipsia, and profound fatigue associated with weight loss. His parents were first cousins. Physical examination revealed clouded sensorium, severe dehydration, fruity-like breath odor, and Kussmaul breathing. The laboratory profile revealed hyperglycemia 21.7 mmol/L with ketonuria, acidosis, serum bicarbonate 6.4 mmol/L, sodium 133 mEql/L, potassium 1.1 mEq/L, and HbA1c 13.2%. On the basis of International …

A Case of Pneumomediastinum: A Rare Complication of Diabetic Ketoacidosis

An 18-year-old male college student with type 1 diabetes of 10 years' duration presented to the emergency department with acute onset of intractable vomiting and retching, which had started earlier the same day. He also described frequent urination and thirst and progressive dyspnea. His recent glycemic control had been poor as a result of frequent missed insulin doses. He had experienced three recent episodes of diabetic ketoacidosis (DKA) in the past year as a result of poor adherence to his basal-bolus insulin regimen. On examination, his blood pressure was 158/88 mmHg, his heart rate was 131 bpm, his respiratory rate was 37 breaths per minute, and his oxygen saturation was 97% on ambient air. His rectal temperature was 99.5°F. He displayed a marked Kussmaul's breathing pattern with a distinctive fruity odor and signs of marked dehydration. Of significance was the incidental finding of bilateral subcutaneous emphysema of the superficial anterior neck. The rest of his examination was unremarkable with no abnormal findings on cardiac or respiratory exam. Hamman's crunch was not observed. Laboratory tests revealed an anion gap metabolic acidosis (anion gap 37 mEq/L, venous pH of 6.98, plasma bicarbonate < 5 mmol/l) and strongly positive blood acetone levels. His blood glucose level was recorded as 806 mg/dl with a serum potassium of 6.6 mmol/l. His leucocyte count was 23.1 with 88% neutrophils, blood urea …

Index of Suspicion in the Nursery

A 5-week-old previously well female born at 41 weeks gestational age presents to the pediatric emergency department in the winter with a 2-day history of poor feeding. Her mother is concerned that the baby is more tired than usual, “is not getting enough to eat,” and is having difficulty latching on to the breast. The mother explains that 2 weeks ago, the infant developed a dry cough and began having emesis after each feeding. She describes the emesis as nonbilious and nonbloody and approximately 1 ounce. An outside pediatrician prescribed a cough and cold medication and told the mother that the emesis was “normal baby spit-up.” Three days ago, the infant developed projectile vomiting immediately following each feeding. Today, the mother reports that the infant is breathing much harder and deeper than usual, with continued and more frequent coughs. She describes the cough as paroxysmal, although she experiences no color changes. The mother is concerned that her baby does not look like herself and is difficult to arouse. A review of systems reveals that the baby has not taken any human milk today, although her urine output has remained the same, with heavy, wet diapers. Her 2-year-old sister, who attends child care, has a cough and upper respiratory tract infection. The infant has no diarrhea, and her bowel movements are normal. There were no complications during the pregnancy. Her birthweight was 2,722 g, and she has been gaining weight appropriately, although the mother describes her as “scrawny” at birth. Physical examination of the infant in the emergency department shows a temperature …

Diabetic ketoacidosis with pneumomediastinum: a case report

An 18-year-old male with type 1 diabetes mellitus presented to the emergency department after one day of lethargy and vomiting. Physical examination revealed a dehydrated male with tachycardia and Kussmaul’s respiration. There was subcutaneous emphysema in both supraclavicular regions. Chest auscultation revealed a positive Hamman’s sign. Laboratory investigation was significant for metabolic acidosis with venous blood pH 7.08. Plasma glucose was 1438 mg/dl; ketones were present in the urine. Chest X-ray showed subcutaneous emphysema and pneumomediastinum, which resolved spontaneously within 72 hours of initiation of treatment for diabetic ketoacidosis.Pneumomediastinum is an uncommon complication of diabetic ketoacidosis. Recognizing that severe diabetic ketoacidosis may cause pneumomediastinum allows for expedient management.

Acute renal failure and neurological manifestations following ingestion of wild mushrooms

Sir, A 58-year-old nonalcoholic man was admitted to the emergency department with one day history of confusion, vomiting, oliguria. He was under no medication or drug abuse. His blood pressure was 140/80 mmHg, pulse rate 80 bpm, body temperature 38°C, and respiratory rate 30 breaths/min. Physical examination was remarkable for pinpoint pupils (miosis) bilaterally; no signs of meningeal irritation were noticed. The patient was lethargic, he obeyed to doctor's commands and communicated with confused conversation, showing disorientation and disorganized thinking (GCS:14). He presented with a deep and labored breathing pattern, such as Kussmaul breathing. He was treated with ceftriaxone 2 g/day, as empirical therapy for bacterial meningitis. The patient was intubated due to impending coma and acute respiratory failure and was transferred to the intensive care unit (ICU). Laboratory data revealed: WBC: 18000/ cm3 with neutrophils 80%; Hct: 38; PLT: 200000; Blood Urea Nitrogen: 110 mg/ dl; Creatinine: 5.2 mg/ dl; Potassium: 4 MEq/l; Sodium: 139 mEq/l; Chloride: 101 mEq/l; SGOT: 19; SGPT: 16; LDH: 459; γGT: 18; total bilirubin: 0.68. Arterial blood gases, under assist control ventilation with FiO2 60%, tidal volume 500 ml και breathing rate 14, were: PO2: 268 mmHg, PCO2: 31 mmHg, PH: 7.32, HCO3: 16. A brain C/T revealed no abnormal signs and a chest C/T showed bibasilar opacities. A lumbar puncture was performed and cerebrospinal fluid (CSF) test results were: White blood cell (WBC): 2/mm3 (28% polymorphs, 72% lymphocytes), protein: 65 g/L, glucose: 85 mg/ dl. Cerebrospinal fluid (CSF) Gram's stain and cultures, and tests for HSV 1 and 2, enteroviruses, Coxsackie viruses, Listeria monocytogenes, CMV and Borelia were all negative. Blood cultures, IgG and IgM antibodies for leptospira interrogans, borellia burgdorferi, brucella, coxiella burnetii and immunologic tests for vasculitis were also negative. Renal ultrasound revealed normal-sized kidneys and no hydronephrosis. The patient was placed on continuous venovenous hemodiafiltration (CVVHFD) due to anuric acute renal failure (ARF) of unknown origin. Ceftriaxone 2 g/d and clindamycin (600 mg/td) were provided for presumed aspiration pneumonia. Renal biopsy showed marked focal interstitial lymphocytic infiltrate, consistent with interstitial nephritis. Two days later, the patient was apyrexial and alert and was successfully extubated after a short weaning trial. He acknowledged having consumed wild, brown-coloured mushrooms two days prior to admission. Two friends of his had tried the same mushrooms, without developing any symptoms. The patient was transferred to a dialysis department; his renal function gradually improved and he was discharged four weeks later in an excellent condition. The medical history and clinical presentation of the patient were consistent with mushroom intoxication. Other causes of interstitial nephritis and altered consciousness such as Wegener's granulomatosis, microscopic polyangiitis, leptospirosis, methanol or salicylate intoxication were excluded. Although the exact type of mushrooms ingested by the patient was not identified, his clinical pattern was similar to intoxication by mushrooms from the genus cortinarius [Figure 1]. This particular type contains the toxin orellanine, which is responsible for acute interstitial nephritis and ARF, while preserving hepatic function.[1] Its oxidation leads to the production of reactive oxygen species and depletion of glutathione, rendering renal cells susceptible to oxidant damage.[2] Figure 1 Mushrooms of genous cortinarius The clinical picture consists of an asymptomatic period, followed by oliguric renal failure 2-20 days postingestion. Common symptoms include nausea and vomiting, neurological manifestations (paraesthesia, cognitive disorders), parasympatheticomimetic reactions (for example, mysis), lumbar and abdominal pains.[1] Wide variations in individual sensitivity are observed and there is no correlation between the amount ingested and the intensity of signs.[3] The high individual sensitivity may suggest that renal toxicity results from the toxin's hepatic metabolism and the hydroxylation capacity of hepatic P450 cytochromes.[4] Additionally, our patient did not mention any use of acetaminophen, which might have depleted glutathione faster and could explain the intoxication. The incidence of renal failure varies from 30-45%,[4] with acute tubulointerstitial nephritis, as the predominant finding in renal biopsy.[1] Recovery of renal function is obtained within a month in 64% of the cases, while in all other cases renal failure persists.[4] Hemodialysis is the only appropriate treatment, which may eliminate the free circulating toxin, while furosemide may aggravate renal lesions.[5] N-acetylcysteine is another reported treatment specific to orellanine intoxication, but its benefit remains debatable.[2,6] In our patient, the syndrome of unexplained tubulointerstitial nephritis with neurological manifestations was finally attributed to cortinarius poisoning. Clinicians should be aware of these potential toxicities that are characterized by high individual sensitivity and may result in permanent renal lesions.

Extreme hyperglycemia with ketoacidosis and hyperkalemia in a patient on chronic hemodialysis

A patient on hemodialysis for end-stage renal disease secondary to diabetic nephropathy was admitted in a coma with Kussmaul breathing and hypertension (232/124 mmHg). She had extreme hyperglycemia (1884 mg/dL), acidosis (total CO(2) 4 mmol/L), hyperkalemia (7.2 mmol/L) with electrocardiographic abnormalities, and hypertonicity (330.7 mOsm/kg). Initial treatment with insulin drip resulted in a decrease in serum potassium to 5.3 mmol/L, but no significant change in mental status or other laboratory parameters. Hemodialysis of 1.75 hours resulted in rapid decline in serum glucose and tonicity and rapid improvement of the acidosis, but no change in mental status, which began to improve slowly after the hemodialysis was stopped, but with ongoing treatment with continuous insulin infusion. The rate of decline in tonicity during hemodialysis (14.5 mOsm/kg/h) was high, raising concerns about neurological complications. In this case, extreme hyperglycemia with ketoacidosis, hyperkalemia, and coma developing in a hemodialysis patient responded to insulin infusion. Monitoring of the clinical status and the pertinent laboratory values is required to assess the need for other therapeutic measures including volume and potassium replacement and emergency dialysis. The indications for and risks of emergency dialysis in this setting are not clearly defined.

„Geisterpeak” in der Gas-Chromatografie bei schwerer metabolischer Azidose

A 31-year-old female with known type 1 diabetes mellitus was referred because of symptomatic hyperglycemia. On admission she was delirious and impressed with marked Kussmaul breathing. All other vital signs were normal. Blood serum glucose concentration was 26.4 mmol/l. Arterial blood gas analysis revealed massive metabolic acidosis (pH 6.80) with an elevated anion gap (21 mmol/l) and a marginally increased osmolar gap (21,5 mOsm/l). Despite normalization of the serum glucose and acidemia after administration of normal saline, insulin and bicarbonate, the delirium persisted, and the possibility of an additional intoxication had to be considered. Serum headspace analysis for intoxication with solvents (gas chromatography) finally detected a "ghost peak", which could not be assigned to any established substance. The same peak was, however, found in a healthy subject's serum and was found to be a "toluene peak". Toluene is contained as "contaminator" in gels in blood collection tubes. The patient gradually regained consciousness and "merely" suffered from diabetic ketoacidosis associated with cocaine use. The differential diagnosis of high anion gap metabolic acidosis includes among other reasons intoxications with different kinds of solvents. When looking for solvents in the serum when poisoning is suspected (headspace analysis), only blood collection tubes without gel (EDTA plasma) should be used, because all gels contain solvents (in this case toluene).

Pharmacology Review: Sodium Phenylacetate and Sodium Benzoate in the Treatment of Neonatal Hyperammonemia

Ammonia is present in all body fluids and exists primarily as ammonium ion at physiologic pH. Hyperammonemia is defined as a blood ammonia concentration greater than about 100 mcmol/L in neonates or 50 mcmol/L in children and adults (precise cut-offs vary, depending on individual laboratory normative ranges). The concentration of ammonia is 10 times higher in tissue than in blood. A 5- to 10-fold increase in blood ammonia concentration usually is toxic to the nervous system. Hyperammonemia in the neonatal period, especially when due to inborn errors of metabolism, can progress rapidly and cause severe neurologic damage or early death. Hyperammonemia can be caused by inborn errors of metabolism as well as by a variety of acquired conditions (Tables 1 and 2). Urgent treatment is required because of the potential for irreversible neurologic sequelae that can, in many cases, be prevented by prompt diagnosis and institution of therapy. | Urea cycle defects | || | Amino acid transporter deficiencies | | Organic acidemias | | Fatty acid oxidation defects | | Pyruvate carboxylase deficiency | | Mitochondrial disorders | | Hyperinsulinism/hyperammonemia syndrome (glutamate dehydrogenase mutations) | | Delta1-pyrroline-5-carboxylate synthase deficiency | Table 1. Inborn Errors of Metabolism Associated With Hyperammonemia | Sampling artifact | || | Cardiovascular | | Perinatal asphyxia | | Liver failure | | Bacterial colonization (urease-positive organisms) | | Iatrogenic | Table 2. Causes of Acquired Hyperammonemia The combination of sodium phenylacetate (NAPA) and sodium benzoate (NABZ) in a 10%/10% solution is an intravenously administered United States Food and Drug Administration (FDA)-approved drug used as adjunctive therapy for …

Severe lactic acidosis and nephrolithiasis in an infant—etiology?: Answer

A 4.5-month-old girl was admitted to the pediatric emergency room with dyspnea and tachypnea. Two weeks prior to admission the patient presented to a local hospital with restlessness and was diagnosed with a urinary tract infection; she later developed gastroenteritis. She was feeding with breast milk only. No history of increased susceptibility to infections was described. Her brother died because of sepsis and metabolic acidosis at the age of three months. There was also consanginuity between the parents. She exhibited Kussmaul breathing with a respiratory rate of 60/min, and tachycardia (176/min) without fever or any finding of heart failure. Height, weight and blood pressure percentiles were in the normal ranges. Marked hepatosplenomegaly was detected on physical examination. The eye examination was normal. Laboratory studies revealed blood pH of 7.05, pCO2 9.6 mm Hg, bicarbonate 2.4 mmol/L, base excess −25.1 mmol/L, sodium 143 mmol/L, potassium 3.9 mmol/L, chloride 94 mmol/L, anion gap 50.5 mmol/L, blood urea nitrogen 15 mg/dL, serum creatinine 0.44 mg/dL, total protein 4.6 g/dL and albumin 3.0 g/dL. Serum had lipemic appearance with a triglyceride level of 1988 mg/dL and cholesterol of 296 mg/dL, HDL 68 mg/dL; SGOT 570 U/L (0–50), SGPT 200 U/L (0–40), total bilirubin 0.15 mg/dL, calcium 9.7 mg/ dL, phosphorus 4.3 mg/dL, uric acid 17.9 mg/dL, ammonia 200 μg/dL, lactic acid 17.3 mmol/L (0.5–2.2), initial blood glucose 63 mg/dL (while hypoglycemia levels of 22 and 35 mg/dL glucose values were obtained during hospitalization period), hemoglobin 10.2 g/dl, WBC 12,200/mm with 56% lymphocyte, thrombocyte count 733,000 mm (control 133,000). Urine pH was 6, specific gravity 1.030; glucose, reducing substances and ketone bodies were negative. Urinary system ultrasonography demonstrated enlarged (80–81 mm) kidneys with normal echogenity and hyperdense areas of 7 mm diameter on left inferior region, 3 mm on middle calicea and 5 mm on right middle calicea; liver 115 mm, spleen 91 mm (Fig. 1). During follow-up she passed a stone, which revealed Weddellite (CaC2O4. 2.25 H20) upon infrared spectroscopy analysis. Amino acid/acylcarnitine profile tests by tandem mass spectrometry were found to be normal.

Think clearly, be sincere, act calmly: Adolf Kussmaul (February 22, 1822-May 28, 1902) and his relevance to medicine in the 21st century.

This past year, 2002, marked the 100th anniversary of the death of Adolf Kussmaul. To rheumatologists, he is important as the author of the first case of idiopathic vasculitis, polyarteritis nodosa, which even today is the basis of our understanding of vasculitis. To general internists, his name is linked to Kussmaul's sign and Kussmaul breathing, and to gastroenterologists, he is in many ways-through the development of the gastric pump and the first gastroscope-the father of modern gastroenterology. His reputation as an excellent teacher, his compassion for his patients, and his ability as a clinician scientist led him to be regarded as a giant of 19th century medicine. Kussmaul's life and career, dedicated foremost to reducing human suffering and advancing medicine as a scientific discipline with a strong humanistic foundation, make him a role model for physicians of today.

Pneumomediastinum in diabetic ketoacidosis

A17-year-old female with type 1 diabetes of six years duration, controlled on a basal-bolus insulin regime (48 units per day) had deliberately stopped her insulin for two days, resulting in diabetic ketoacidosis (DKA). Examination revealed the patient had Kussmaul (acidotic) breathing with respirations of 40 per minute; she was dehydrated with a strong odour of ketones on the breath. The pulse rate was 150 per minute (ECG: sinus tachycardia), BP 90/55 mmHg, oral temperature showed hypothermia, 34.2oC. The patient complained of precordial pain and auscultation revealed a clearly audible retrosternal ‘crackle’, particularly well heard at the left sternal edge. Laboratory investigations showed a plasma glucose of 30 mmol/L, plasma bicarbonate 2 mmol/L, sodium, potassium and urea of 121, 5.7 and 8 mmol/L respectively, and an arterial pH of 6.8. Routine haematology showed a marked leucocytosis (41 x 10 /L: 89% neutrophils) and blood cultures subsequently grew beta-haemolytic streptococci. The chest X-ray showed features of pneumomediastinum and pneumopericardium with subcutaneous emphysema in the right axilla and supra-clavicular fossae (see figure 1). Treatment consisted of intravenous saline and subsequently dextrose-containing fluids with appropriate potassium supplementation and a low-dose sliding scale insulin regime. Immediately after initial blood cultures were taken, intravenous ceftriaxone was started. By 48 hours the patient’s general condition had improved, the biochemical parameters were normal, the chest pain and the precordial ‘crackle’ sound had disappeared, as had the radiological signs of the pneumomediastinum. The patient was restarted on subcutaneous insulin regime.