Presented by Amy McCroskey, MD
History and Physical
A 4-year-old boy presented to the emergency department with difficulty in breathing for about 3 hours. The mother provided the history, because the patient was unable to answer questions, due to his difficulty in breathing. She stated that for the past 5 days he had a nonproductive cough, sneezing, and nasal drainage, without a fever. Also, he had been vomiting for the last 3 days about 3 to 4 times a day, no blood or bile present. He had diarrhea and was urinating more frequently. She did not know the quantity or color of his bowel movements or urine. He had diffuse abdominal pain. Mom noticed a decrease in his appetite and he had not been able to tolerate any food for the past day, but he was tolerating fluids. She thought that he was loosing weight, and that he appeared to be more thirsty than normal. She said that his symptoms have progressively worsened, and today she noticed he was having difficulty breathing. She did not give him any medications, and denied any possible ingestion. She denied that the boy had ever had a similar illness, and she denied any sick contacts.
Past Medical History: ED visit 2 months prior foreign body removed from nose
Past Surgical History: None
Social history: up-to-date immunizations, stays at home with mother and does not attend day care
Family History: Uncle- diabetes on dialysis, mother hypertension
VS: BP 104/62 HR 120 RR 38 Temperature 37.0 Oxygen Sat 100% on room air, weight 14.1 kg (weight 2 months prior 18 kg)
General: Patient was alert, not speaking, but looking at people when they talked to him, and he would respond by nodding his head. He appeared to be in mild respiratory distress, and appeared weak while lying on the stretcher.
HEENT: Head: Normocephalic, atraumatic Ears: tympanic membrane clear Eyes: pupils are equally round and reactive to light, & extraocular eye movements are intact Nose: minimal nasal discharge Throat: dry mucous membranes, saliva foaming at corners of the mouth, no tonsillar erythema, exudate or enlargement
Lungs: Clear to auscultation bilaterally. No wheezing or crackles. Good air entry bilaterally. Labored, irregular breathing pattern. Using abdominal, and accessory muscles to breath.
Cardiovascular: Tachycardic, normal S1& S2, no murmurs
Abdomen: Soft, nontender on palpation, mildly distended, bowel sounds present, no guarding or rigidity
Extremities: Able to move all extremities without any difficulty, movements were sluggish.
Skin: No bruising, rashes, or petechiae
Neurologic exam: Not answering questions, decreased response to pain (noticed when IV was inserted), and responded to verbal stimuli with eye opening
Capillary blood gas: pH 7.00 / PCO2 19.3 / PO2 64.9 / bicarb 4.5 / K 6.0 / Lactate 3.5
ED blood glucose meter >600
Color: clear, yellow
Epithelial cells <5
Leukocyte Esterase Negative
Urine Specific Gravity 1.039
CBC: WBC 36.8 Hemoglobin 16.5 Hematocrit 44.4 platelet count 332
Lytes: Na 137 K 4.9 Cl 100 CO2 <5 BUN 13 Cr 0.8 Ca 9.4 Mg 2.2
Phos. 4.3 Glucose 770
1. What is the most likely diagnosis?
a. Dehydration secondary to gastroenteritis
c. Toxic ingestion
d. Diabetic ketoacidosis
e. Acute respiratory failure
2. What is the estimated fluid deficit in this patient, and how should this deficit be managed?
a. Estimated fluid deficit 2%, give initial bolus of 1 mL/kg of 0.9 NaCl
b. Estimated fluid deficit 20%, give initial bolus of 10 mL/kg of 0.9 NaCl
c. Fluid deficit 5-10% initial 10-20 mL/kg bolus of 0.9 NaCl
d. Fluid deficit of 10%, give initial bolus of 10-20 mL/kg of lactated ringers
e. Fluid deficit of 15-20%, give initial bolus of 10 mL/kg of 0.45 NaCl and start and insulin infusion
3. What treatment can lead to volume overload, accelerated hypokalemia, hypernatremia, and paradoxical CNS acidosis, and associated with a fourfold increase in the development of cerebral edema
c. potassium replacement
d. 0.9 NaCl fluid resuscitation
1. D. Diabetic Ketoacidosis
This patient had variety of symptoms but there were a few key points in the history and physical that made DKA more likely. He was among the 27% to 40% of new-onset diabetics who present in DKA. It is characterized by hyperglycemia, ketonemia, ketonuria, & metabolic acidosis (pH <7.30, Bicarbonate <15 mEq/L). DKA is caused by an insulin deficiency resulting in the inability of cells to take up and use glucose. This causes many hormones to be upregulated to increase the production of glucose, and to decrease the glucose utilization by cells.
The clinical manifestations of DKA are related to the degree of dehydration, hyperosmolarity, and the severity of acidosis. The assessment of severity is based on clinical and laboratory findings. The neurologic status (alert, lethargic, comatose) should be assessed because severe neurologic compromise at presentation is a poor prognostic indicator, and brain edema should be considered. Other factors that influence the severity are compromised circulation, the acid base status (Kussmaul breathing: deep and labored breathing pattern to compensate for metabolic acidosis), anion gap, volume status, and the duration of symptoms such as polyuria, polydipsia, polyphagia, weight loss, enuresis, anorexia, vague abdominal discomfort (in theory may be caused by gastric distention or stretching of the liver capsule), visual changes, and candidiasis. This patient was probably in moderate to severe DKA.
Other laboratory tests that can be sent in the ED for new onset diabetes are Islet cell autoantibodies, insulin, and C-peptide levels. Islet cell autoantibodies indicate that type 1 diabetes is more likely than type 2. Insulin and C-peptide levels are lower in children presenting with type 1, but there is large overlap so these levels are often not helpful in differentiating early type 1 from type 2.
There are other conditions that should be considered in this patient such as gastroenteritis, toxic ingestion, and infection. Dehydration secondary to gastroenteritis is not the most likely diagnosis, but the patient may have gastroenteritis as an underlying cause of the DKA. In this case the dehydration was mainly secondary to the osmotic diuresis from the glucose drawing water, and electrolytes out of the circulation into the urine. Poor intake and vomiting can produce profound dehydration and electrolyte imbalances, and so the resulting metabolic alkalosis from vomiting and diarrhea may my mask the severity of the acidosis in DKA with a relatively normal pH. Also, ketoacidosis can occur in any condition where there is prolonged vomiting or excessive fasting, but the glucose will not be elevated in those conditions. The sodium is normally high when patients are dehydrated from gastroenteritis. In this case the sodium level was normal. In DKA the sodium level is often normal or low in the presence of significant dehydration because it is affected by hyperglycemia causing osmotic diuresis. A dilutional hyponatremia is created due to water flowing from cells into vessels to decrease the osmolar gradient. The urine specific gravity, is also a sign of volume depletion but it should not be used as a measure of hypovolemia in diabetics because glucose and the ketones raise the specific gravity (concentrated urine vs dilute urine).
Sepsis is unlikely due to the relatively normal vital signs. The leukocytosis is common in DKA and it reflects the degree of ketosis instead of the presence of infection. On the differential there may be an elevated neutrophil count in DKA but there will often be an elevation of band neutrophils if there is infection. Toxic ingestion of ethylene glycol, isopropyl alcohol, or salicylates should be considered especially in teenagers, when new onset diabetes is less likely. In this case the high anion gap was due most likely to the ketones, and lactate.
2. C. 5-10% deficit, bolus 10-20% NaCl
It is difficult to clinically assess the degree of dehydration in children presenting with DKA. The most widely accepted initial management of children with moderate or severe DKA should be based on an estimated 5-10% fluid deficit of total body weight. The vitals signs and mental status are the best way to estimate the severity of the DKA and thus estimate the fluid deficit. It is recommended to give a bolus of 0.9% NaCl at 10 mL/kg for those children who are not in shock, and 20 mL/kg for those who are in shock. Once the VS are stable, it is important to correct the fluid deficit slowly in children, especially if there is a high calculated osmolality. The goals of initial isotonic volume expansion are to restore an effective circulating volume by replacing sodium and water loss, and restore GFR to enhance clearance of ketones and glucose from the blood. Some clinicians prefer to avoid lactated ringers because the lactate is rapidly converted into bicarbonate, and administration of free bicarbonate during DKA is not generally recommended. An initial insulin bolus is not longer recommended.
• Calculate 5-10% fluid deficit of total body weight
• Bolus 10-20 mL/kg 0.9 NaCl over first hour (10 mL/kg not in shock, 20 mL/kg in shock)
• Depending on the severity of the DKA the fluid deficit can be corrected over 24-48 hours
• In children it is recommended to replace the remaining fluid deficit over 48 hours, to prevent cerebral edema
After the initial fluid bolus then an insulin infusion along with maintenance fluids should be started. The goal is for the glucose level to fall by 50-100 mg/dL per hour to prevent intracerebral osmolar shifts. If the glucose level is decreasing too rapidly decrease the rate of insulin infusion and fluids, or change to D5W 0.45% NaCl. When serum glucose decreases to 250- 300 mg/dL, then change to D5W in 0.45% NaCl, allowing or continuous administration of insulin which is necessary to correct the residual ketoacidosis.
Don’t follow the glucose concentration as a measure of improvement of DKA. Most of the time the hyperglycemia corrects before the ketoacidosis. The anion gap should be monitored. If acidosis is not resolving the patient may need more insulin. Monitor glucose every hour and electrolytes ever 3-4 hours, and replace electrolytes such as potassium appropriately.
• An initial insulin bolus should not be given
• Infusion at 0.1 unit/kg per hour or a lower dose of 0.05 unit/kg/hour may be used in younger children who may be more sensitive to insulin
• The insulin can be mixed in 0.45% NaCl and administered with an infusion pump, and the solution should be concentrated as much as possible (1 unit insulin/ 1 mL of IV fluid)
• Within 60 minutes, the steady state in serum are reached (100 to 200 microU/mL)
Now glucose and ketone production is suppressed, overcome the insulin resistance, peripheral glucose and ketones are metabolized
Discontinue the insulin infusion
• Serum anion gap reduced to normal
• pH is >7.30 or serum HCO3 >15 meq/L
• Plasma glucose <200
Monitor glucose every hour and electrolytes ever 3-4 hours, and replace electrolytes such as potassium appropriately.
3. B Bicarbonate
The use of bicarbonate therapy along with fluid replacement and insulin therapy is not recommended for children presenting in DKA. There has not been any improvement in outcome, and it has been associated with a fourfold increase in developing cerebral edema, along with other complications.
There are many theoretical causes of cerebral edema. Bicarbonate therapy may contribute by causing a paradoxical CNS acidosis. When acidemia is rapidly corrected the respiratory compensation (Kussmaul breathing) is suppressed. There is also a rapid rise in carbon dioxide which is the break down product of bicarbonate, and it permeates the blood brain barrier, causing paradoxical CSF acidosis. Slowly over time the bicarbonate crosses the BBB to provide adequate buffering. Other theoretical causes of cerebral edema are insulin therapy and rapid rate of fluid administration which cause a change in brain osmolarity.
Some physicians recommend the administration of mannitol at the fist sign of altered mental status in children being treated for DKA. Cerebral edema should be considered when the patient remains comatose or relapses into coma after the reversal of acidosis. It can be evident 6-10 hours after the initiation of therapy, without any warning signs and the mortality is 90%. Subclinical cerebral edema in children is probably very common, and may occur prior to or after the onset of therapy.
There are other complications of bicarbonate therapy. One is that the rapid correction of acidosis may result in accelerated hypokalemia, by the potassium being driven into cells and exchanged in the kidney. Another is that the additional sodium load can further increase the degree of hyperosmolality before decreasing glucose levels with fluid and insulin therapy, and cause hypernatremia. It can also eventually produce alkalosis, which can induce dysrhythmias mainly through its effect on the distribution of electrolytes.
• Conservative fluid replacement, and no bicarbonate treatment in children with DKA due to the increased risk for cerebral edema
• Monitor mental status, glucose every hour, electrolytes and anion gap every 3-4 hours,
• Differential diagnosis for DKA: gastroenteritis, surgical abdomen, toxic ingestion, hyperosmolar nonketosis, sepsis
- Initial fluid management of diabetic ketoacidosis in children. Source: The American journal of emergency medicine (Am J Emerg Med) 2000 Oct; 18(6): 658-60
- APLS : The Pediatric Emergency Medicine Resource. By Marianne Gausche-Hill, Susan Fuchs, Loren Yamamoto, Gary R. Strange, American Academy of Pediatrics, American College of Emergency Physicians
- The Johns Hopkins Hospital: The Harriet Lane Handbook 18th Edition
- Emergency Medicine A Comprehensive Study Guide. Tintinalli
- Rosen’s Emergency Medicine
This case discussion presented by Amy McCroskey, MD
Filed under: Intern Report |