23 Flashcards
Emergency conditions causing altered mental status
4 broad categories
Hypoxia, shock, hypoglycemia, and poisoning (or toxic ingestion) are conditions that can present with altered mental status. All must be reversed quickly to prevent cellular damage.
Hypoxemia, shock, and hypoglycemia are each an example of “lack of cellular substrate,” which, if not treated emergently, can lead to cell death:
Oxygen is obviously a critical substrate that must be maintained.
Shock (septic, hypovolemic, cardiac) results in an inadequate perfusion of substrate (oxygen and nutrients) that must be treated immediately.
Glucose is a critical substrate, the absence of which can lead to altered mental status and cell death.
Poisoning causes an intoxication process that can be reversed immediately by specific antidotes.
CNS causes of altered mental status 5
Each one of these etiologies can present with altered mental status:
Seizures
Generalized seizures can result in decreased level of consciousness.
Tumor
Increased intracranial pressure due to mass effect from a tumor can result in progressive behavioral changes and altered mental status.
Subarachnoid hemorrhage
This causes severe headache.
Some patients may also have altered mental status.
Meningitis
Causes increased intracranial pressure and decreased responsiveness.
Trauma
Child abuse and shaken baby syndrome may lead to intracranial bleeds, resulting in a continuum of signs from decreased alertness to complete unresponsiveness and deep coma.
Diff dx for lethargy 9
Sepsis
The combination of fever, lethargy, tachypnea, and decreased urination points to sepsis, or even septic shock.
Sepsis occurs from overwhelming infection—whether bacterial, viral, or fungal.
Meningitis
Hallmark symptoms of meningitis are fever, headache, stiff neck, altered mental status, and photophobia, although many patients present with only two or three of these clinical indicators.
Encephalitis
Encephalitis is often caused by viral infections in children, and presents with altered mental status and fever.
Toxic ingestion
Overdoses (toxic ingestion) often cause otherwise unexplained lethargy.
Depending on the toxin, decreased urine output, rash, and tachypnea may be seen.
Pneumonia
Fever and tachypnea are found with pneumonia
Altered mental status would be uncommon unless the patient was severely hypoxic.
CNS tumor
Increased intracranial pressure from a CNS tumor may lead to lethargy and tachypnea.
Diabetic ketoacidosis (DKA)
DKA can present with lethargy and tachypnea.
Hypoglycemia
Hypoglycemia is a cause of lethargy or altered mental status.
Renal failure
Decreased urine output points strongly toward renal failure.
An associated acidosis could lead to tachypnea and lethargy.
Best way to assess circulation 2
Heart rate is a very sensitive measure of volume status. Never overlook tachycardia; this is the first and most subtle sign of possible inadequate perfusion. It is the most commonly missed finding in patients who have been sent home and return with serious illness.
Capillary refill time is also a sensitive sign of hypovolemia.
Shock
Definition
Compensatory mechanisms in children
Definition
Shock is defined physiologically as inadequate delivery of substrates and oxygen to meet the metabolic needs of tissues:
As cells are starved of oxygen and substrate, they can no longer sustain aerobic oxygen production.
Eventually, cellular metabolism is no longer able to generate enough energy to power the components of cellular homeostasis, leading to disruption of cell-membrane ionic pumps.
The cell swells, the cell membrane breaks down, and cell death occurs.
Compensatory Mechanisms in Children
In the pediatric age group, shock is not a diagnosis based on blood pressure. Children can maintain a normal blood pressure until they are in profound shock. Children in shock have excellent compensatory mechanisms to maintain tissue perfusion that include:
Increased heart rate (tachycardia): Because cardiac output is dependent on both stroke volume and heart rate, the body typically tries to maintain cardiac output when stroke volume decreases by increasing the heart rate.
Increased systemic vascular resistance (vasoconstriction).
Increased heart contractility: Resulting in more complete emptying of the ventricles.
Increased venous tone: Results in more blood return to the heart.
Increased respiratory rate (tachypnea): The body’s attempt to compensate for the metabolic acidosis caused by decreased oxygen perfusion of the tissues and cells.
Therefore, in early shock you will find the following: elevated heart and respiratory rates, peripheral blood vessel constriction (causing cool, clammy extremities and delayed capillary refill time), and decreased peripheral pulses (due to vasoconstriction and decreased stroke volume). The vasoconstriction can lead to difficulty obtaining a pulse oximeter measurement.
Important to Remember
Because children compensate so well in early shock, hypotension is a late sign of shock.
4 types of shock
Which are most common in children
Distributive (Includes neurogenic and anaphylactic; some authors also include septic shock in this category) All of these conditions are characterized by an intravascular hypovolemia caused by: Vasodilation Increased capillary permeability Third-space fluid losses Hypovolemic Most common type of shock worldwide.
Results from inadequate fluid intake to compensate for fluid output (e.g., vomiting, diarrhea, hemorrhagic fluid loss).
Signs and symptoms include:
Mental status changes Tachypnea Tachycardia Hypotension Cool extremities Oliguria
Cardiogenic
Rare in children, but may be associated with the following conditions:
Severe congenital heart disease
Dysrhythmias
Cardiomyopathy
Tamponade
Signs and symptoms include:
Cool extremities Delayed capillary refill (> 2 seconds) Hypotension Tachypnea Increasing obtundation Decreased urine output Septic Results when infectious organisms release toxins that affect fluid distribution and cardiac output.
Can result from bacterial, viral, or—in immunocompromised patients—fungal infections.
Patients in septic shock typically require repeated boluses of fluid. They may also need medications (epinephrine, norepinephrine or dopamine) to enhance cardiac contractility and to vasoconstrict the vessels.
It is important to realize that patients in septic shock may present initially as compensated or "warm" shock, with the following findings: Warm extremities Bounding pulses Tachycardia Tachypnea Adequate urination Mild metabolic acidosis Hypovolemic (hemorrhage, diarrhea/dehydration) and septic shock are the most common causes of shock in children.
Administration of fluids in shock
Maintaining perfusion always trumps everything else in fluid management.
In shock, intravascular volume replacement is the priority. Fluid replacement should be performed with isotonic solutions (e.g., normal saline), not with hypotonic fluids, and the rate of infusion should be as fast as possible.
This is true even in patients who have a relative contraindication to receiving large amounts of fluid (such as patients with meningitis, where the risk of increased intracranial pressure exists).
When the patient is no longer in shock, then fluid restriction may be instituted.
What access should be placed when many attempts to place an IV is missed
Placement of an intraosseous line is easy and fast, and this type of line may be used to administer any fluid.
If a peripheral intravenous line cannot be placed within 90 seconds, an intraosseous line is the fastest way to get access.
An intraosseous needle is inserted into the marrow cavity of a long bone. Substances are then injected into the bone marrow, where they are absorbed almost immediately into the general circulation.
Although placing a central venous line (A) is not wrong, this technique actually has more risks involved than trying to place an intraosseous line. Also, placement of a central line, such as a subclavian line, takes too long in infants and young children and has a high morbidity. In an older child like Sarah (or in an adult), however, a central line is acceptable if it can be placed within 90 seconds.
An arterial line (D), such as in the radial artery, is not the right choice because arteries cannot tolerate the massive fluids used during a fluid resuscitation and this may impair the overall circulation.
NG (C) or PO (E) fluids are unlikely to be absorbed from the stomach when perfusion is impaired and will take too long.
Differential Dx of fever and petechiae rash 5
Meningococcal sepsis
Whenever a patient presents with fever and petechiae, this diagnosis must always be at the top of the list.
This is true even if the patient otherwise looks well.
A blood culture must always be done and antibiotics must always be given until the disease can be definitely ruled out.
Kawasaki disease
Kawasaki disease is associated with fever and a rash.
The mucocutaneous lesions include:
A “strawberry” tongue
Dry, red, cracked lips
Diffuse erythema of the oral cavity
Erythema and/or edema of hands/feet
A polymorphic truncal rash
Toxic shock syndrome
Toxic shock syndrome causes fever and a sunburn-looking rash that might feel rough to the touch (like sandpaper).
Rocky Mountain spotted fever (RMSF)
RMSF causes fever and petechiae as well.
The petechiae tend to be on the palms and soles.
RMSF is epidemiologically less likely than meningococcus unless in an endemic area.
Scarlet fever
Scarlet fever starts as a finely punctate pink-scarlet exanthem.
Rash appears on the upper trunk 12-48 hours after the onset of fever.
As the exanthem spreads to the extremities, it become confluent and feels like sandpaper.
It fades in 4-5 days and is followed by desquamation of the skin.
Linear petechiae are evident in body folds and are called Pastia’s sign.
The pharynx is beefy red and the tongue is initially white and rough (strawberry tongue); within 4-5 days the white coating sloughs off and the tongue becomes bright red.
Meningococcal disease Epi RF Transmission Disease course/ signs Mortality Sequalae
Meningococcal Disease
Epidemiology
The incidence of meningococcal disease varies by age and location.
In the U.S., annual incidence varies from 0.5 to 1.5 cases per 100,000 persons.
Infection with Neisseria meningitidis has become the leading cause of bacterial meningitis in children since the introduction of the Hib vaccine and is an important cause of septicemia.
Although outbreaks can occur in institutions such as child care centers, schools, colletes, and military recruit camps, fewer than 5% of cases overall are associated with outbreaks.
Peak incidence occurs in children < 12 months of age, with another peak at age 16 through 21 years.
Serogroups B, C, and Y each account for approximately 30% of total reported cases.
Among young adults, mosts cases are caused by serogroups C, Y, or W-135, strains that are potentially preventable with currently available vaccines.
In infants, 50% to 60% of cases are caused by serogroup B, for which there is no available vaccine available in the U.S.
Risk Factors
Persons living in close accommodations (students in dormitories, military recruits in boot camp)
Complement deficiency
Anatomic or functional asplenia
Transmission
The disease is transmitted through respiratory droplets and requires close person-to-person contact with an infected individual.
The incubation period is 1-10 days
Disease Course
Acute systemic meningococcal disease is most frequently manifested by three syndromes:
Meningitis
Meningitis with accompanying meningococcemia
Meningococcemia without clinical evidence of meningitis
The course of disease can be quite varied, ranging from insidious to abrupt. The following are common early signs:
Fever Chills Malaise Myalgia Prostration Rash (can be macular, maculopapular, petechial, or purpuric, and may be difficult to distinguish from that of a viral infection) Signs of more fulminant disease:
Purpura Limb ischemia Coagulopathy Pulmonary edema Shock Mortality
Coma and death can ensue within hours despite appropriate therapy.
Overall case-fatality rate is 10%, and is higher in adolescents.
Sequelae
Sequelae occur in 11% to 19% of survivors and include:
Hearing loss
Neurologic disability
Loss of digit/s or limb/s
Scarring
Fluid management in septic shock
Enhancing perfusion is the critical goal in this situation.
A patient with septic shock often needs repeated boluses of fluid. Give as much fluid as is needed to attain perfusion.
After a certain point, you may need inotropes to enhance cardiac contractility and vasopressors to raise the blood pressure by vasoconstricting the vessels. Epinephrine and dopamine are acceptable choices.
You do not want to slow the fluids unless the physical signs show good perfusion (normal pulse, capillary refill, and blood pressure). (SIADH (syndrome of inappropriate antidiuretic hormone) is a complication of meningitis, but perfusing the patient is more important.)
A diuretic should be given only if the patient is well perfused and has signs of fluid overload (such as rales on the lung exam).
Work up for suspend meningococcal sepsis
Tx
Because sepsis is at the top of your differential, it needs to be ruled out with a CBC, gram stain, and cultures (A) as soon as possible.
Hypoglycemia and other electrolyte imbalances are common causes for altered mental status, and these must be checked in a chemistry panel (C).
You want to start antibiotics as soon as possible; blood and urine should be drawn before starting the medications.
At this time, there is no indication to do a CT scan (B) or a lumbar puncture (LP) because the patient is unstable.
Empiric coverage for suspected meningococcemia is ceftriaxone.
If suceptabilities dictate, the most appropriate antibiotic treatment for meningococcemia is often Penicillin G:
Pediatric dose: 250,000-300,000 units/kg/day (maximum 12 million units per day) divided every 4-6 hours
Adult dose: 12-24 million units daily divided every 4-6 hours
Once a definitive diagnosis of meningococcal disease is made, one can switch to penicillin G and successfully eradicate the organism from the blood and CSF. However, penicillin does not eliminate the carrier state. Therefore, at the end of the penicillin therapy, the patient will need to be treated with either rifampin (children or young adults) or ciprofloxacin (adults). Alternatively, a patient can be treated 5 to 7 days with ceftriaxone, which also eliminates the carrier state.
Guidelines for meningococcal prophylaxis
Close contacts warrant prophylaxis with antibiotics.
In adults, ciprofloxacin is the drug of choice.
Rifampin, ceftriaxone, and azithromycin are alternatives.
Neither rifampin nor ciprofloxacin are recommended for pregnant women.
In children (< 18 years old), either oral rifampin or intramuscular ceftriaxone may be used for prophylaxis. Prophylaxis is also recommended for those health care workers who had intimate exposure (such as occurs with unprotected mouth-to-mouth resuscitation, intubation, or suctioning before antibiotics are administered).
Household, childcare, and nursery school contacts are considered high risk.
What can kidneys undergo during shock
Underperfusion of the kidneys secondary to shock can cause pre-renal failure. It is common to misinterpret an elevated BUN and creatinine in this situation as renal failure and withhold fluids from a poorly perfused patient.
Remember that perfusion takes precedence in fluid management.
Meningococcal conjugate vaccine MCV4
For the general population, the MCV4 is given to children ages 11-18.
Normally given intramuscularly during the routine preadolescent immunization visit (at 11-12 years).
A booster dose should be given at age 16.
For adolescents who receive the first dose at age 13 through 15 years, a one-time booster dose should be administered, preferably at age 16 through 18 years, before the peak in increased risk.
Adolescents who receive their first dose of MCV4 at or after age 16 years do not need a booster dose.
There is no routine recommendation for any of the licensed meningococcal vaccines for healthy children younger than 11 years of age.
College freshmen living in dorms and those in the military are considered high risk and should receive a dose of the tetravalent conjugate (MCV4) vaccine.
