Intern Report Case Discussion 1.14

intern-report

Presented by Alison Loynd, DO

HISTORY

A 35-year-old female is transferred from an urgent care center by EMS with chief complaint of altered mental status and fever. The patient is unable to answer questions. She is approximately 18 weeks pregnant and febrile. She has no nausea, vomiting, dyspnea or noted seizure activity. Her boyfriend reports that the patient was previously healthy. She had a dental extraction approximately one month prior. Since that time, she has had pain all over, headache, nausea and vomiting. She was seen in the ED one week ago and given antibiotics for dental infection. The patient has been taking antibiotics as prescribed for the last week.  She went to the dentist office today complaining of headache and facial swelling. At the clinic, she had a procedure done but the boyfriend does not know any more specifics. He reports that afterwards she was unable to ambulate and felt dizzy and weak.  Due to her changes in mental status, they called 911.

PMH: None per friend.
PSH: None per friend.
GYN: G1P0 currently 18 weeks pregnant with routine prenatal care.
Meds: Cephalexin and Amoxicillin x 1 week.
Allergies: None known
Social: She does not drink, smoke or use illicit drugs.

PHYSICAL EXAM

GENERAL: The patient is obtunded, at times somnolent but arousable to her name. She opens her eyes and moves extremities spontaneously. She is making no vocalizations.
VITALS: BP 145/85  HR 121  RR 20 Temp 39.2 R  94%RA
HEENT: Head is atraumatic, normocephalic. TM clear and intact bilaterally, no effusion or hemotympanum. PERRLA. 2mm bilaterally. Mucous membranes are dry. No tonsillar edema or exudates. There is some mild edema of the left mandible, it is not indurated or fluctuant. Left mandible and cheek are tender to palpation. Neck is supple. Trachea midline with no lymphadenopathy.
HEART: Tachycardic and regular No murmur, gallop or rub.
LUNGS: Clear to auscultation bilaterally with shallow breathing
ABD: Soft. Gravid. Fundus palpable below umbilicus. Bowel sounds are hyperactive.
EXT: No edema or cyanosis. She has full range of motion spontaneously. Pulses present and equal bilaterally.
SKIN: Hot and dry. No noted edema, cyanosis or rash.
NEURO: Patient has a GCS of 11 (3E, 2V, 6M). She is opening her eyes, initially following simple commands, moves spontaneously. She is not vocalizing. She has an intact gag. Face appears symmetrical. Her patellar and Achilles reflexes are normal with no clonus.

LABORATORY EVALUATION
CBC: WBC 23.8 (22.4 Neutrophils) / Hgb8.8/ Hct 26.7/ Platelets 352
LYTES: Na 133/K 3.2/HCO 19/BUN 6/Cr 0.6/Glucose 130   Mag 1.5 Ca 8.2
CSF: Hazy, 750 RBC, 700 nucleated cells, 93 N, 5 L, glucose < 20, protein 122
GS: No organisms on gram stain. Numerous PMNs, mod RBC
UDS Positive for cannibis

Bedside US: Active intrauterine fetus, heart rate 178. Gestational age 19 weeks by femur length and 20 weeks by fundal height.

QUESTIONS

1.    Considering your differential evaluation, what is most likely in this patient?
A.    Trauma
B.    Encephalitis/meningitis
C.    Brain Abscess
D.    Preeclampsia
E.    Saggital sinus thrombosis

2.    What is your diagnostic test of choice?
A.    CT with and without contrast.
B.    LP and serology.
C.    CT without contrast.
D.    Obtain 24 hour urinalysis, liver function and platelets.
E.    MRI.

3.    Treatment considerations include:
A.    Anticoagulation with heparin.
B.    Antiepileptic prophylaxis – IV phenytoin.
C.    Multiple antibiotics: IV Penicillin, Metronidazole, Ceftriaxone and glucocorticoid.
D.    Antihypertensive – IV hydralazine.
E.    Single antibiotic regimen – IV Clindamycin

Discussion

1. Considering your differential evaluation, what is most likely in this patient?

C. Brain Abscess. Our patient was found to have a brain abscess. Brain Abscess is a focal collection within the brain parenchyma that may arise as a complication of infections, trauma, or surgery. Up to 60 percent of cases come from direct spread via subacute or chronic otitis media, mastoiditis, sinusitis or dental infection. Foreign bodies can also cause abscess by acting as a nidus for infection. Finally, direct spread can complicate neurosurgical cases. Abscess occurring from bacteremia usually results in multiple abscesses mostly along the distribution of the middle cerebral artery. 20-40 percent of brain abscess will have no identified etiology.

Symptoms commonly include a headache, usually localized to the side of the abscess, with gradual or sudden onset. The pain tends to be severe and not relieved by typical over-the-counter pain medications. Changes in mental status range from lethargy progressing to coma and stupor and are indicative of severe cerebral edema. This is a poor prognostic sign. Patients with cerebral edema will frequently have associated nausea and vomiting.

Physical exam may include fever, however fever is unreliable as it is not always or even commonly associated with brain abscess. Focal neurologic deficits are observed in approximately fifity percent of patients. Deficits may include aphasia, anopsia, muscle weakness, hemiparesis, nystagmus or ataxia.

Your differential may have included trauma, encephalitis/meningitis, intoxication, preeclampsia, seizure and cerebral venous thrombosis. This patient had no known falls or accidents and was in a stable monogamous relationship making trauma and domestic violence unlikely. In any pregnant or postpartum patient, preeclampsia should be considered. She was observed at a medical clinic prior to EMS transfer and no seizure activity was noted. The patient’s urinalysis was negative for protein and she did not have edema, hypertension or hyperreflexia. Cerebral venous thrombosis is an uncommon entity but is a consideration in pregnant patients or women using hormonal birth control. Patients may present with headache, nausea, vomiting, focal neurological deficit and variations in mental status. The recent dental work followed by development of symptoms makes brain abscess more likely than cerebral venous thrombosis.

2. What is your diagnostic test of choice?

A. Diagnostic testing includes CT with and without contrast. CT scan must be done first. Only after a CT scan has ruled out cerebral edema can a lumbar puncture be preformed due to the risk of increased ICP leading to herniation.

Acutely, an abscess may be difficult to recognize on CT as it can be poorly demarcated and is associated with localized edema. There will be evidence of acute inflammation but no visible tissue necrosis. After two to three weeks, as the disease progresses, necrosis and liquefaction occur, and the lesion becomes more visible as surrounded by a fibrotic capsule.

A lumbar puncture is indicated and can be done only after a CT scan has been completed. Most initial CT scans do not identify the abscess. The LP is useful as your differential includes meningitis or encephalitis. The CSF pattern is variable and similar to meningitis showing elevated protein, decreased glucose and an elevated white cell count.

Definitive diagnosis of brain abscess may require direct examination of brain tissue obtained by open or stereotactic brain biopsy under the direction of an experienced neurosurgeon. A CT scan of the brain without contrast is done to evaluate the patient for acute intracranial hemorrhage but is insufficient evaluation alone.

This patient’s symptoms do not represent preeclampsia or eclampsia, thus HELLP evaluation of serology and urinalysis is not necessary though should be included in the evaluation of any obtunded pregnant patient. Preeclamspia may present at any time during pregnancy and into the postpartum period. An OBGYN consult should still be done in this pregnancy, but may be done on a routine basis when the patient is stabilized as the fetus is not viable at this gestational age. This patient does not appear to have any trauma and does not need general surgery.

An MRI is also a valid test for brain abscess, thought the patient’s stability and general medical condition must be weighted against the time delay required for proper imaging and availability of the MRI. CT with and without contrast is faster and more widely available on an emergent basis. The MRI can be obtained later if necessary.

3. Treatment considerations include:

C. Treatment requires a combination antimicrobial therapy and glucocorticoids. Definitive treatment usually requires eventual drainage.

Microbiology is variable and depends on the primary site of infection. In some cases, identification of the organism may provide a more information on the primary site or underlying condition yet undiagnosed. Commonly identified pathogens include Streptococcus species and anaerobes such as fusobacterium and enterobacterium commonly due to origination from oral flora.  As with any infection, immunocompromised hosts can present with a wide variety of infectious bacteria, parasites and fungi. Immigrants or foreign travelers may be infested with parasitic infection such as neurocystercercosis.

Current recommendations for an abscess from an oral, ear or sinus source calls for Metronidazole (15mg/kg IV load followed by 7.5mg/kg IV q 6-8hrs) PLUS Penicillin (24 million units daily divided into six doses) PLUS Ceftriaxone (2gm IV every 12 hours). Nafcillin (2gm IV every four hours) or Vancomycin (30mg/kg IV daily divided according to renal function) should be included in any patients for whom S. aureus bacteremia is considered or in patients with a history of penetrating trauma
Antibiotics that do not cross the blood brain barrier should not be used. This includes Aminoglycosides, Erythromycin, Tetracyclines, Clindamycin and the first generation cephalosporins.

Duration of therapy is prolonged, usually six to eight weeks. Further management is geared by follow-up assessment of the clinical course and repeat imaging. Indications for surgical excision include lack of clinical progress or deterioration, increased intracranial process (cerebral edema, intracerebral pressures), or progressive increase in the ring diameter.
Adjunctive use of glucocorticoids should be considered if the patient has signs of cerebral edema, depressed mentation or mass effect demonstrated on imaging.

Our patient’s course:

She was immediately admitted to Neurosurgical care for further management with presumed diagnosis of meningitis vs encephalitis based on her initial head CT. While in the Emergency Department, she did deteriorate from somewhat responsive and following commands to stupor and only minimal response to painful stimuli.

CT 1: Head without contrast: Loss of the gray-white matter interfaces in the left cerebral hemisphere, left frontotemporal parietal area. Effacement of the sulcal and gyral markings.  There is very mild compressive effect on the left frontal horn and body of the lateral ventricle. There is no uncal herniation. There is note of a phlegmonous appearing tissue in the left masticator space.

CT 2: CT Head with IV contrast: Noted difference from noncontrast scan is erosive changes in the left superior molar alveolar ridge appears related to the inferior aspect of the masticator space abscess.

On hospital day 3, follow-up CT #3: showed development of a large intraparenchymal abscess of the left temporal and parietal areas. Etiology was presumed to be from a dental infection eroding thru the bone and leading to masticator muscle abscess seeding to the brain.

The patient continued to deteriorate, undergoing surgical debridement complicated by intracranial hemorrhage. She remains alive today, minimally interactive with her environment requiring fulltime nursing care. She continues to be managed by an  Obstetrician for her developing and apparently healthy fetus and has reached 35 weeks gestation under their close observation.

References:
Southwick, Frederick (May 2009) Treatment and Prognosis of Brain Abscess UpToDate
Southwick, Frederick (May 2009) Pathogenesis, Clinical Manifestations, and Diagnosis
of Brain Abscess UpToDate
Thomas, Lisa (May 2009) Brain Abscess Emedicine

This case discussion presented by Alison Loynd, DO

Intern Report Case 1.14

intern-report

Presented by Alison Loynd, DO

HISTORY

A 35-year-old female is transferred from an urgent care center by EMS with chief complaint of altered mental status and fever. The patient is unable to answer questions. She is approximately 18 weeks pregnant and febrile. She has no nausea, vomiting, dyspnea or noted seizure activity. Her boyfriend reports that the patient was previously healthy. She had a dental extraction approximately one month prior. Since that time, she has had pain all over, headache, nausea and vomiting. She was seen in the ED one week ago and given antibiotics for dental infection. The patient has been taking antibiotics as prescribed for the last week.  She went to the dentist office today complaining of headache and facial swelling. At the clinic, she had a procedure done but the boyfriend does not know any more specifics. He reports that afterwards she was unable to ambulate and felt dizzy and weak.  Due to her changes in mental status, they called 911.

PMH: None per friend.
PSH: None per friend.
GYN: G1P0 currently 18 weeks pregnant with routine prenatal care.
Meds: Cephalexin and Amoxicillin x 1 week.
Allergies: None known
Social: She does not drink, smoke or use illicit drugs.

PHYSICAL EXAM

GENERAL: The patient is obtunded, at times somnolent but arousable to her name. She opens her eyes and moves extremities spontaneously. She is making no vocalizations.
VITALS: BP 145/85  HR 121  RR 20 Temp 39.2 R  94%RA
HEENT: Head is atraumatic, normocephalic. TM clear and intact bilaterally, no effusion or hemotympanum. PERRLA. 2mm bilaterally. Mucous membranes are dry. No tonsillar edema or exudates. There is some mild edema of the left mandible, it is not indurated or fluctuant. Left mandible and cheek are tender to palpation. Neck is supple. Trachea midline with no lymphadenopathy.
HEART: Tachycardic and regular No murmur, gallop or rub.
LUNGS: Clear to auscultation bilaterally with shallow breathing
ABD: Soft. Gravid. Fundus palpable below umbilicus. Bowel sounds are hyperactive.
EXT: No edema or cyanosis. She has full range of motion spontaneously. Pulses present and equal bilaterally.
SKIN: Hot and dry. No noted edema, cyanosis or rash.
NEURO: Patient has a GCS of 11 (3E, 2V, 6M). She is opening her eyes, initially following simple commands, moves spontaneously. She is not vocalizing. She has an intact gag. Face appears symmetrical. Her patellar and Achilles reflexes are normal with no clonus.

LABORATORY EVALUATION
CBC: WBC 23.8 (22.4 Neutrophils) / Hgb8.8/ Hct 26.7/ Platelets 352
LYTES: Na 133/K 3.2/HCO 19/BUN 6/Cr 0.6/Glucose 130   Mag 1.5 Ca 8.2
CSF: Hazy, 750 RBC, 700 nucleated cells, 93 N, 5 L, glucose < 20, protein 122
GS: No organisms on gram stain. Numerous PMNs, mod RBC
UDS Positive for cannibis

Bedside US: Active intrauterine fetus, heart rate 178. Gestational age 19 weeks by femur length and 20 weeks by fundal height.

QUESTIONS

1.    Considering your differential evaluation, what is most likely in this patient?
A.    Trauma
B.    Encephalitis/meningitis
C.    Brain Abscess
D.    Preeclampsia
E.    Saggital sinus thrombosis

2.    What is your diagnostic test of choice?
A.    CT with and without contrast.
B.    LP and serology.
C.    CT without contrast.
D.    Obtain 24 hour urinalysis, liver function and platelets.
E.    MRI.

3.    Treatment considerations include:
A.    Anticoagulation with heparin.
B.    Antiepileptic prophylaxis – IV phenytoin.
C.    Multiple antibiotics: IV Penicillin, Metronidazole, Ceftriaxone and glucocorticoid.
D.    Antihypertensive – IV hydralazine.
E.    Single antibiotic regimen – IV Clindamycin

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Intern Report Case Discussion 1.13

intern-report

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
Medications: none
Allergies: 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

Physical Exam
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
Neck: supple
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

Laboratory Results

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
Urinanalysis:

Color: clear, yellow

Epithelial cells <5
Glucose 3+

Leukocyte Esterase Negative
Ketone 3+

WBC <5
pH 5.0

RBC 2-5
Urine Specific Gravity 1.039

Bacteria none
Blood 1+

Nitrite negative
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
Acetone 2+
Osmolarity 342

ECG

ECG

Questions

1.    What is the most likely diagnosis?
a.    Dehydration secondary to gastroenteritis
b.    Sepsis
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
a.    insulin
b.    bicarbonate
c.    potassium replacement
d.    0.9 NaCl fluid resuscitation
e.    Phosphate

Discussion

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.

Fluid administration
•    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.

Insulin Infusion
•    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.

Key Points
•    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

References

  • 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
  • Up-to-Date

This case discussion presented by Amy McCroskey, MD

Intern Report Case 1.13

intern-report

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
Medications: none
Allergies: 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

Physical Exam
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
Neck: supple
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

Laboratory Results

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
Urinanalysis:

Color: clear, yellow

Epithelial cells <5
Glucose 3+

Leukocyte Esterase Negative
Ketone 3+

WBC <5
pH 5.0

RBC 2-5
Urine Specific Gravity 1.039

Bacteria none
Blood 1+

Nitrite negative
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
Acetone 2+
Osmolarity 342

ECG

ECG

Questions

1.    What is the most likely diagnosis?
a.    Dehydration secondary to gastroenteritis
b.    Sepsis
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
a.    insulin
b.    bicarbonate
c.    potassium replacement
d.    0.9 NaCl fluid resuscitation
e.    Phosphate

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Intern Report Case Discussion 1.12

intern-report

Presented by Samuel Lee, MD

H&P

A 3 year old African-American male is brought to the ED by his mother with a fever for six days, sore throat, and a rash on his chest.  The patient had been seen by his PCP 3 days ago, diagnosed with scarlet fever, and started on amoxicillin.
Since then the fever has not subsided and the mother has noticed painful swelling and skin peeling over the patient’s lips, palms, soles, and genital area.  The patient cries when walking and avoids placing weight on his soles.  The mother denies any sick contacts.  The patient does not have a cough, nausea, vomiting ,or diarrhea.  He has been eating and drinking, and the mother states that he is still producing urine.

Past Medical History: multiple past ED visits for croup
Medications: Amoxicillin X 3 days
Allergies: None
Immunizations: UTD
Social Hx: lives with mother and grandmother in an apartment
Birth History: Full term SVD

Physical Exam:
Vital Signs: BP 90/56, HR 136, RR 24, Rectal Temp 38.8, Oxygen Sat. 99% on Room air; weight 18 kg
General: The patient is sitting on his mother’s lap; awake and alert, good eye contact; cries if he is made to stand on his feet
HEENT: Atraumatic/normocephalic; PERRL, bilat conjunctival injection, no discharge. The peri-oral area is swollen and erythematous and the lips are cracked. There is pharyngeal erythema with no exudate, vesicles, or lesions seen. MMM. No LAD upon palpation. Neck is supple; there is no nuchal rigidity.
Resp: Lung sounds clear to auscultation. No wheezing/rales/rhonchi.
Chest: Sandpaper rash on chest and upper abdomen which is resolving per mother.  No vesicles or lesions.
CV: RRR, no murmurs, rubs, or gallops; pulses 2+ and equal in all ext.
ABD: Soft, nontender/nondistended.  Positive bowel sounds, no flank tenderness.
EXT: palms and soles are swollen, erythematous, tender to palpation. No vesicles or lesions present. Cap refill less than 2 sec.
GU: There is an erythematous rash and peeling skin on the groin and penis. Testes descended.
Neurological: Awake, alert; able to ambulate but cries when weight is placed on soles.

Impression: Three year old male with 6 day hx of fever and scarlitiniform rash, initially diagnosed as scarlet fever; Condition has not improved with amoxicillin. Now with conjunctival injection, erythema and skin peeling of lips, palms, and GU area.

Lab studies
CBC: WBC 10, Hemoglobin 11.2, Hematocrit 32.6, Platelets 328
Diff: Neutrophils 61%, Lymphocytes 22%, Monocytes 14%, Eosin 3%, Bands 1%
Electrolytes: Na 138, K 4.8, Cl 103, CO2 20, AG 15
BUN 5, Creatinine 0.4
Glucose 110
CRP 75
UA: clear, yellow, Specific Gravity 1.016, pH 7.5, WBC 5-10, no RBC, Nitrite and LE negative; 0 bacteria
CXR: mild hyperinflation, no focal opacity
Rapid Strep test neg
EKG: NSR@100 bpm, no axis deviation, no PR prolongation, no QRS widening, no atrial or ventricular hypertrophy, no ST changes, no T wave inversions, no accessory waves or ectopic beats; no previous EKG available for comparison

QUESTIONS:

1. Given this patient’s history and physical exam, what is the best definitive course of action?

a. Admit the patient for treatment and arrange for an echocardiogram
b. Continue supportive treatment as an outpatient and have the patient follow up in one week for an echocardiogram
c. Initiate antibiotic treatment for Urinary Tract infection and arrange for a voiding cystourethrogram
d. Advise the patient’s mother to continue with amoxicillin and follow up with her PCP in 2 days.

2. What is a serious complication of this patient’s diagnosis?

a. Development of meningitis in the next week
b. Coronary artery aneurysm and myocardial infarction
c. Pyelonephritis
d. Rhabdomyolysis and acute renal failure

3. What is the definitive treatment for this patient’s condition?

a. IV fluid 20cc/kg bolus
b. Nitrofurantoin 2 mg/kg PO X 10 days
c. IVIG 2 mg/kg over 12 hrs, Aspirin 100 mg/kg/day divided qid
d. Acetaminophen 15 mg/kg

ANSWERS:

1. A. The patient fulfills diagnostic criteria for Kawasaki disease and should be admitted for treatment and echocardiogram evaluation.  Sterile pyuria is commonly seen, and with negative LE, nitrite, and bacteria in the urine, treatment is not warranted.  Continuing amoxicillin therapy will not be effective in treating this patient.

2. B. In Kawasaki disease the most life-threatening complication is coronary artery involvement and subsequent infarction.  This patient did not exhibit any meningeal signs or AMS, so meningitis would not be in your differential.  The sterile pyuria and hand/foot swelling and pain can be attributed to Kawasaki disease.

3. C. IVIG and ASA is the definitive treatment for Kawasaki disease.  IV hydration or acetaminophen may be used as supportive treatment but will not treat the underlying cause.

DISCUSSION:

Kawasaki disease is a pediatric vasculitic syndrome which was first documented in 1967 by Dr. Tomisaku Kawasaki.  He had observed that some pediatric patients with a self-limiting fever and rash would subsequently die of myocardial infarctions.  Later studies showed that a significant number of patients with the particular constellation of symptoms of prolonged fever, rash, oral involvement, and conjunctivitis developed coronary artery aneurysms either during or soon after their illness.  Today Kawasaki disease is the most common cause of acquired pediatric heart disease in developed nations.

Kawasaki disease outbreaks occur in three-year cycles and are typically seen during the influenza season of late-winter to early-spring.   The disease causes immune-mediated damage to the body’s vasculature, with the most alarming complication being coronary artery involvement which can lead to aneurysms and myocardial infarction.

The diagnosis of Kawasaki disease is based on the clinical presentation and requires a fever greater than 39° C for at least five days in addition to four of the five following symptoms:

  1. Conjunctival injection, usually non-exudative
  2. Cervical lymphadenopathy of at least 1.5 cm diameter
  3. Lip and oral cavity involvement such as swollen or dry lips, erythematous tongue, or pharyngeal erythema
  4. Trunk or genital area erythema
  5. Hand or foot erythema, swelling, or desquamation

Additional clinical findings may include sterile pyuria, hepatitis, gall bladder distention and hydrops, and swelling or erythema at a previous BCG vaccination site.

The clinical course of Kawasaki disease follows three distinct phases.  The acute phase begins with onset of the fever and symptoms.  This phase typically lasts one to two weeks.  Cardiac complications during this first phase are aneurysm, pericarditis, and myocarditis.  The subacute phase begins when the fever and symptoms begin to disappear.  This phase lasts approximately one to three weeks, and thrombocytosis and cardiac complications such as coronary artery aneurysms and myocardial infarction can occur.  The convalescent phase begins when all symptoms disappear and ends when serum CRP and ESR levels return to normal.  The majority of coronary aneurysms are discovered during this phase, which typically lasts four weeks.

Over the past few years the diagnosis of Incomplete Kawasaki disease has become established in emergency medical practice to guide practitioners on the care of patients who fit some but not all the criteria.  For patients with 5-day fever and 3 of the 5 symptoms, if the patient is less than 6 months old then treatment is warranted.  For those patients who are older than 6 months or those who fulfill only 2 of the additional criteria, CRP and ESR levels are drawn.  If CRP ❤ mg/dL and ESR< 40 mm/h, then the patient is monitored for any progression of new symptoms.  If CRP >3 and ESR >40, then a CBC, albumin, ALT, and urinalysis are all examined.  If any three or more of the following studies are abnormal, then the patient is treated for Kawasaki disease:

  • Albumin<3
  • Anemia
  • WBC>12,000
  • Elevated ALT
  • Platelets>450,000 after 7 days of fever
  • Pyuria

However, if less than three of the studies are found to be abnormal, then the patient undergoes an echocardiogram.  Abnormal echo results would warrant starting treatment.

The treatment of Kawasaki disease focuses on blocking the immune-mediated damage to the vasculature.  IVIG at a dose of 2 mg/kg is infused over 12 hours.  If the fever and other symptoms do not begin to subside, a repeat dose can be given.  Aspirin 80 mg/kg/day divided into four doses Q6 is also given for its anti-platelet effects.  A 12-lead ECG and echocardiogram should also be done to assess for any cardiac involvement.  In addition to basic bloodwork to establish a diagnosis of Kawasaki or incomplete Kawasaki disease, baseline levels of CRP and ESR should be noted as well.

Back to our patient…

Clinical Course:

The patient was admitted and started on IVIG 36 mg over 12 hours and ASA 1800mg PO divided qid.  The fever subsided and the erythema began to resolve.  Echocardiogram showed a normal ventricular size and function and no effusion.  The coronary arteries were well visualized and were of normal size.  The patient was afebrile for 36 hours and was stable for discharge with low-dose aspirin for 8 weeks and followup with Pediatric cardiology in 2 weeks.
At the clinic two weeks later, the patient was asymptomatic.  ESR was 11 and CRP was 1.85.  A repeat ECG and Echocardiogram were normal.  Repeat followup in 1 year.

Clinical Pearls:

  • Kawasaki disease is diagnosed by 5-day fever greater than 39º C, plus four of the following: conjunctival injection, lip or pharyngeal erythema, cervical LAD >1.5 cm, rash or peeling of the trunk or genital area, or hand or foot erythema, swelling, or peeling.
  • Complications of Kawasaki disease include coronary artery aneurysm, myocardial infarction, thrombocytosis, sterile pyuria, and gall bladder hydrops.
  • Patients who do not fulfill the criteria for Kawasaki disease may warrant treatment if they are diagnosed with incomplete Kawasaki disease.
  • Ensure prompt follow-up of pediatric patients with fever and URI symptoms who are being discharged from the ED and educate caretakers about Kawasaki disease symptoms.

This case discussion presented by Samuel Lee, MD