16 Flashcards
Glasgow coma scale
The Glasgow Coma Scale (GCS) was initially formulated to assess depth of coma after head injury in adult patients and is the most commonly accepted method for assessing patients with an altered level of consciousness. Level of consciousness describes the patient’s capacity for arousal or wakefulness, and reflects the patient’s present cortical function.
Scoring
Using the Glasgow Coma Scale, a score is assigned in each of three categories:
Best eye-opening response
Best verbal response
Best motor response
These three scores are then added together to come up with the patient’s total score.
Eye-Opening Response 4 - Eyes open spontaneously 3 - Eyes open to verbal command 2 - Eyes open to pain 1 - No eye opening
Verbal 5 - Oriented 4 - Confused, but able to answer questions 3 - Inappropriate words 2 - Incomprehensible sounds 1 - No verbal response
Motor
6 - Obeys commands
5 - Localizes pain
4 - Withdraws from pain
3 - Abnormal flexion, decorticate posture
2 - Extensor response, decerebrate posture
1 - No motor response, flaccid
With a total possible score of 15, patients with a GCS of 8 or less may require aggressive intervention and management.
Adjusted verbal response criteria for children under the age of 5 years:
5 - Smiles, orientated to sounds, follows objects, interacts
4 - Cries but consolable, inappropriate interactions
3 - Inconsistently inconsolable, moaning
2 - Inconsolable, agitated
1 - No verbal response
Vomiting and AMS diff dx
Condition Discussion
Diabetic ketoacidosis (DKA)
Vomiting—usually precipitated by the acidosis—is often a presenting symptom, as are increased respiratory rate and vague abdominal pain.
A preceding history of enuresis and polydipsia is strongly suggestive of newly presenting diabetes.
Unless a coincident infection precipitates ketosis and thus a presentation for medical evaluation, one does not expect to see fever in a child with DKA.
Diffuse abdominal pain is characteristic, a consequence of the ongoing acidosis.
Significant dehydration is a prominent feature due to a combination of vomiting and osmotic diuresis.
Altered mental status is often a result of dehydration and/or electrolyte abnormalities; its presence should make one consider whether or not there is concurrent cerebral edema.
Tachypnea is a normal physiologic response to attempt to compensate for the acidosis in DKA, which is purely a metabolic acidosis.
Toxic ingestion
Toxic ingestion often results in vomiting, altered mental status, and obtundation.
Dehydration is possible depending on the extent of vomiting and the degree to which any change in mental status impairs oral intake.
Aspirin overdose may present with tachypnea.
Abdominal pain may be seen in toxic ingestions—in an overdose of iron, for example.
Gastrointestinal obstruction
Vomiting, sometimes bilious, is commonly seen in GI obstruction.
Almost all patients with obstruction will be dehydrated; the degree of dehydration depends on degree of vomiting.
Abdominal pain is a prominent feature of GI obstruction.
Altered mental status is unlikely unless dehydration is severe.
Increased intracranial pressure (ICP)
Increased ICP often presents with vomiting.
Rarely, a tumor might cause a central diabetes insipidus.
A patient with increased ICP may exhibit an altered level of consciousness, often preceded/accompanied by headache.
Gastroenteritis
Gastroenteritis is the most common cause of vomiting; it may be viral or bacterial.
It usually also presents with fever, colicky abdominal pain, and diarrhea.
Dehydration is common in gastroenteritis.
Appendicitis
Abdominal pain is a prominent symptom of appendicitis, classically migrating to the RLQ.
Vomiting also may be seen, but is not as prominent as the pain.
Bacterial pneumonia
The possibility of pneumonia should be investigated in any child presenting with abdominal pain (can be caused by inflammation of the pleura).
If the patient becomes septic, can see a diminished level of consciousness.
Signs of dehydration, if present, are mild.
Pyelonephritis
Vomiting may be seen in pyelonephritis and may lead to dehydration.
It would be important to distinguish between urinary frequency—which one might expect in the case of pyelonephritis—and polyuria, which should not commonly be present.
Dx DM 3 criteria
The American Diabetes Association outlines four ways to diagnose diabetes mellitus:
A patient may be diagnosed with diabetes if he/she has symptoms of diabetes (polyuria, polydipsia, and unexplained weight loss) plus a random (any time of day, without regard to time since last meal) plasma glucose concentration > 200 mg/dL (11.1 mmol/L).
A patient can also be diagnosed with diabetes mellitus with a fasting (no caloric intake for at least 8 hours) blood glucose > 126 mg/dL (7.0 mmol/L).
A patient can also be diagnosed with diabetes mellitus with a 2-hour postload glucose of > 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test.
Finally, in 2010 the ADA also voiced a position statement advocating for the use of hemoglobin A1c (HbA1c) values in the diagnosis of diabetes. A HbA1c ≥ 6.5% in an adult is diagnostic of diabetes. The test should be performed in a laboratory using a method that is National Glycohemoglobin Standardization Program (NGSP)-certified and standardized to the Diabetes Control and Complications Trial (DCCT) assay. (Many assays in common clinical use do not meet these criteria.)
In the absence of unequivocal hyperglycemia or symptoms, these results should be confirmed by repeating on a different day.
Dx DKA 3 criteria
The presentation of vomiting, tachypnea, mental status changes, and dehydration points to a diagnosis of DKA. The diagnostic criteria for DKA are:
A random blood glucose of > 200 mg/dL (> 11.1 mmol/L)
A venous pH < 7.3 or serum bicarbonate < 15 mEq/L (< 15 mmol/L), and
Moderate or large ketonuria or ketonemia.
Early management considerations in DKA Meds Admit or not Consult or not Lab work
Given severe dehydration and the risk of cerebral edema, vital signs should be monitored frequently and observed for signs of further deterioration or improvement with therapy. Expecting that you will have labs back confirming the diagnosis of DKA well within the hour, it is appropriate to start planning anticipated therapies.
Insulin Administration
Fluid resuscitation itself will help lower the blood glucose, but only insulin will correct the metabolic derangements of DKA by suppressing lipolysis and ketogenesis.
An insulin drip (0.1 units/kg/hour) should be started after the patient has received initial volume expansion, usually about 1 hour after starting fluids. (An insulin drip is typically started at the same time as maintenance plus replacement IV fluids.)
Bicarbonate should not be given routinely because of the well-described paradoxical CNS acidosis and hypokalemia from rapid correction of acidosis. In addition, bicarbonate administration has been associated with an increased risk of cerebral edema, the most common cause of diabetes-associated death in children.
Although potassium should be added eventually to the IV fluids, it should not be added until the serum potassium level is known.
An insulin bolus is generally not recommended in children because it has also been associated with an increased risk of cerebral edema and could cause the glucose to drop too rapidly.
After the initial fingerstick, glucose levels should be monitored carefully (every 30 minutes to 1 hour initially).
Hospital Admission
In general, a patient in DKA should be admitted to a hospital unit with experienced nursing staff trained in the monitoring and management of children with DKA and the capability of obtaining frequent and timely physical assessments and laboratory tests. Children with altered mental status, persistent hypovolemia, and those at increased risk for cerebral edema should be considered for admission to the intensive care unit.
Consultation
An endocrinologist is generally involved in the care of all children in DKA.
Labwork
Baseline serum osmolality should be measured prior to initiation of treatment.
A baseline CBC with differential, recommended to help identify an infection as a precipitating factor, should be interpreted with caution, recognizing that the WBC count might be elevated with a left shift due to the stress of DKA alone.
Blood and/or urine cultures should be considered, especially with mental status changes, borderline hypotension, and tachycardia.
Blood lactate, pyruvate, and ammonia levels are not necessary because there is an explanation for altered mental status in a patient with DKA.
In addition, measurement of blood beta-hydroxybutyrate concentrations, when available, are useful to confirm ketoacidosis, and can be used to monitor response to therapy.
DKA
epi
Sxs
Pathophys
Epidemiology
Although usually occurring in patients with type 1 diabetes, DKA can occasionally be found in patients with type 2 diabetes.
There is wide geographic variation (15-70% in Europe and North America) in the frequency of DKA at onset of diabetes, and rates inversely correlate with the regional incidence of type 1 diabetes.
Presentation
DKA should be suspected in pediatric patients who present with the following signs and symptoms:
Vomiting Weight loss Dehydration Shortness of breath Abdominal pain, or Change in the level of consciousness. DKA may be misdiagnosed as the "flu" in patients with new-onset diabetes. A patient with known diabetes who has been vomiting should be assumed to be in DKA until proven otherwise.
Pathophysiology
Type 1 diabetes is caused by a relative or absolute deficiency of insulin. Insulin facilitates the entry of glucose into peripheral tissues, and inhibits lipolysis, glycogenolysis, and tissue catabolism.
The lack of insulin and excess counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone) causes a catabolic state characterized by increased gluconeogenesis, lipolysis, and glycogenolysis, and an inhibition of glycolysis, which result in hyperglycemia and ketogenesis.
The increased lipolysis leads to increased mobilization of free fatty acids, which are then converted into ketones (acetoacetic and beta-hydroxybutyric acids).
The increased production of ketones lowers the blood pH, and leads to metabolic acidosis, which is worsened by lactic acidosis from dehydration and poor tissue perfusion.
When circulating blood glucose levels reach ~180 mg/dL, an osmotic diuresis occurs, leading to hypovolemia, dehydration, and a loss of sodium, potassium, and phosphate in the urine.
Intravascular volume depletion stimulates catecholamine release, which causes further lipolysis. The osmotic diuresis and hyperglycemia cause serum hyperosmolarity. Dehydration can result in renal impairment, which will exacerbate hyperglycemia.
What kind of respiration s seen during DKA
With Kussmaul respirations, there is a pattern of rapid and deep breathing because the patient is attempting to blow off the excess CO2 caused by their metabolic acidosis.
These respirations are distinctive because other causes of tachypnea-such as heart and lung disease-reduce vital capacity, leading to rapid, shallow respirations, not deep.
Lab abnormalities in DKA 8
pH on a venous blood gas decreased
This will be low because of the metabolic acidosis caused by the elevated ketoacids in the blood.
Serum sodium decreased
Hyponatremia results from the osmotic movement of water into the extracellular space in response to the hyperglycemia and hyperosmolarity (dilutional hyponatremia), as well as from increased renal sodium losses.
It is important to calculate the corrected sodium and monitor how it changes with therapy.
Potassium normal
Although total body potassium will always be depleted through urinary losses, Isabella’s serum potassium level can be high, normal or low.
The acidosis and insulinopenia that is present in DKA drives potassium out of the cells and into the serum. As the acidosis is corrected with treatment, her serum potassium will always drop, reflecting her true total body levels.
This drop needs to be anticipated and the potassium prevented from dropping to dangerously low levels; potassium needs to be monitored carefully.
Potassium is usually added to the IVF after initial volume expansion and after urine output is established, unless there are EKG changes (peaked T waves).
Potassium can be given as potassium chloride, potassium acetate, and/or potassium phosphate; the use of potassium phosphate reduces the amount of chloride the patient is given, thus decreasing the risk for causing an iatrogenic hyperchloremic acidosis, and provides both potassium and phosphorus, both of whose total body stores are often low at presentation of DKA.
Bicarbonate decreased
This will be low because of the metabolic acidosis caused by the elevated ketones and lactic acid in the blood.
Creatinine elevated
Even though renal function may be normal, the creatinine can be elevated due to the severe dehydration (also termed prerenal azotemia).
Serum glucose elevated
By definition, this is elevated in diabetes and DKA.
Serum ketones elevated
Serum ketones, or a serum beta-hydroxybutyrate level, will be elevated. These will be followed closely to determine how the patient responds to insulin therapy.
Urine ketones elevated
These will be elevated, too, as serum ketones spill over into the urine.
Urine ketones should be monitored with every void until they clear.
Calculate adjusted serum sodium in DKA
Sodium decreases by 1.6 meq/L for each 100 mg/dL rise in glucose. Therefore, to calculate an adjusted serum sodium in the presence of hyperglycemia:
Corrected sodium = [{(measured glucose - 100) / 100} x 1.6] + measured sodium
Types of dehydration 3
There are three types of dehydration, depending on the level of the serum sodium. Checking the serum sodium is one of the most important reasons for obtaining electrolytes in any child presenting with dehydration.
Isotonic/Isonatremic (Na = 130-150 mEq/L [130-150 mmol/L])
This is the most common type of dehydration in children and occurs when sodium and water losses are balanced, including children presenting with acute gastroenteritis and diarrhea.
Typically the deficit in isonatremic dehydration can be replaced over 12 hours.
Hypotonic/Hyponatremic (Na < 130 mEq/L [< 130 mmol/L])
This type of dehydration occurs when sodium losses exceed those of water.
This most commonly occurs when patients consume diluted fluids or water in the face of dehydration.
Hyponatremia may also be the result of adrenal insufficiency.
The deficit in hyponatremic dehydration is typically replaced evenly over 24 hours.
Rapid correction of hyponatremia is associated with central pontine myelinolysis (a neurologic disease caused by damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons, the most common cause of which is the too-rapid correction of hyponatremia.
Hypertonic/Hypernatremic (Na > 150 mEq/L [> 150 mmol/L])
This type of dehydration occurs when water losses exceed that of sodium and is associated with the highest mortality.
Possible causes of hypernatremic dehydration include breastfeeding failure, use of inappropriate rehydration solutions (boiled milk), and diabetes insipidus.
The deficit in hypernatremic dehydration is typically replaced evenly over 48 hours.
Too-rapid correction of hypernatremia is associated with the development of cerebral edema.
Note: Although our patient is hyponatremic secondary to hyperglycemia, she best fits into hypertonic dehydration secondary to the osmotic diuresis and the resulting hyperosmolarity. Therefore, patients with DKA typically have their fluid deficit replaced evenly over 48 hours.
Basic steps of fluid management 4
- Provide bolus fluids to restore intravascular volume
This is accomplished with a 10-20 mL/kg bolus of 0.9% saline (isotonic or “normal” saline). The general recommendation for patients who are not in DKA or renal failure is to provide serial boluses until the patient urinates. However, patients in DKA typically start urinating very shortly after providing fluid boluses due to osmotic diuresis (this occurs in diabetes when the serum glucose concentration exceeds the renal threshold for glucose reabsorption [> 180mg/dL], leading to glucosuria and obligate loss of water, sodium and potassium, not because they have received enough resuscitation fluids. Therefore, patients in DKA should be monitored for improvement of their vital signs (normalized heart rate and blood pressure) and mental status.
2. Correct dehydration
The amount of fluid required to replace the patient’s deficit is dictated by your assessment of the degree of dehydration (3–5%, 6–10% or 11–15%). The composition of fluid (0.3% saline, 0.45% saline, 0.9% saline, etc.) and rate of infusion is dictated by the serum sodium concentration/osmolarity. In hyponatremic dehydration a sodium deficit is calculated, and in hypernatremic dehydration a free water deficit is calculated.
3. Provide maintenance fluids
In addition to the fluids required to replace the fluid deficit, patients with dehydration must also be provided with maintenance fluids. Maintenance fluids replace daily insensible losses (perspiration and respiration) and normal urine output (approximately 2.0 mL/kg/hr for children < 15 kg and 1.0 mL/kg/hr for children > 15 kg and adults). Insensible losses account for approximately 40% of daily maintenance needs, while normal urine output accounts for about 60%. In general, 0.25% saline (1/4 normal saline) or 0.45% saline (1/2 normal saline) with 5-10% dextrose is used to provide maintenance fluids.
4. Replace ongoing losses
In many patients with dehydration, the losses may continue, even after replacement therapy has begun. Therefore, careful attention must be paid to monitoring the patient’s output and vital signs, to determine the need for additional replacement. The amount and type of replacement fluid is determined by the source of the losses. For example, in gastroenteritis with ongoing diarrhea, stool output that exceeds 1.0 g/kg/hr should be replaced every 4 to 6 hours with 0.45% saline (1/2 normal saline). Additional examples of ongoing losses are emesis, nasogastric tube output, increased insensible losses due to fever, and tachypnea.
Estimate free water deficit
Dr. Sato tells you: “Think of Isabella’s body as a big bag of water. Remember that: 1 gram of water = 1 mL of water; and so, 1 kg of water = 1 liter of water.
Thus, for Isabella: If her currently weight is 22 kg and she is 10% dehydrated, then her pre-illness weight can be calculated with the following formula:
Pre-illness weight = Current weight / [(100 - % dehydrated) x 0.01] = 22 / [(100-10) x 0.01] = 24.44 kg.
Deficit = 24.44 kg (pre-illness weight) - 22 kg (current weight) = 2.44 kg of body weight = 2440 mL of estimated free water deficit.
In most situations, the composition of the fluid and the amount of time over which it is given will depend on the serum sodium concentration and osmolarity. In DKA, however, the deficit is replaced evenly over 48 hours secondary to the hyperosmolarity.
Calculate daily maintenance flu
There are three methods of calculating maintenance fluids:
By caloric expenditure
By body surface
The Holliday-Segar method
The Holliday-Segar method is probably the easiest to remember.
100 mL/kg/day for the first 10 kg of body weight
50 mL/kg/day for the second 10 kg of body weight
20 mL/kg/day for each additional 1 kg of body weight
Go by pre illness weight
Complication of DKA
Inappropriate slowing of heart rate - increased ICP distort the vagus nerve and cause heart rate to decrease, and a rising blood pressure in response to that are signs of cerebral edema and increased intracranial pressure. There needs to be a high index of suspicion for the development of cerebral edema with at least hourly monitoring of vital signs and neurologic status, and treatment should be given as soon as the diagnosis is suspected (i.e., slow the rate of fluid administration, intravenous mannitol, transfer to ICU).
Cerebral Edema
Symptomatic cerebral edema is a relatively rare (0.5-1% of pediatric DKA episodes) complication of DKA management. Unfortunately, this complication is associated with high rates of mortality (21-24%) and morbidity.
Timing
Cerebral edema can occur at any point during the management of DKA. It can occur even before treatment is initiated and up to 24 hours after initiation of treatment.
Pathophysiology
The pathophysiology of cerebral edema is poorly understood, but epidemiologic research has identified several risk factors:
High BUN concentration at presentation
Profound acidosis with hypocapnia
Attenuated rise in the measured serum sodium with treatment, and
Administration of bicarbonate.
Admission orders
ADC VANDISMAL
A =Admit (floor, room, service, attending, resident)
D=Diagnoses (list in order of priority)
C=Condition (good, fair, guarded, critical)
V=Vitals (q 2 hrs, q shift, routine)
A=Activity (ad lib, bed rest, up to chair, walk 3x/d)
N=Nursing (ins and outs, drains, wound care, etc.)
D=Diet (regular, low sodium, diabetic, NPO, etc.)
I=IV fluids (type and rate)
S=Studies (imaging, EKG)
M=Medications (include both scheduled and prn)
A=Allergies (drug or food)
L=Labs (CBC, lytes, cultures, etc.)
