Markovchick Vincent J., Pons Peter T., Bakes Katherine M.(ed.) Emergency medicine secrets. 5th ed
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Chapter 58 HEAT ILLNESS408
n
Heat cramps—painful involuntary spasms of large muscle groups, usually occurring after
strenuous exercise
n
Heat tetany—occurs in the setting of heat stress with hyperventilation; presents with
carpopedal spasms, perioral and peripheral paresthesias
n
Heat syncope—dehydration from intense sweating, followed by peripheral vasodilation and
decreased motor tone
n
Heat exhaustion—excessive dehydration and electrolyte depletion; precursor to heat stroke
n
Heat stroke—life-threatening condition in which the body loses its ability to control its
temperature
Some have advocated for describing heat illness in basically two categories: heat stroke and
heat exhaustion (with heat exhaustion essentially including everything that does not qualify as
heat stroke).
7. How are heat cramps treated?
Heat cramps are treated with oral salt solutions or intravenous saline. Passive stretching of
the affected muscles may also help relieve the cramps.
8. What are the symptoms of heat syncope and how is it treated?
Patients with heat syncope have a sudden onset of lightheadedness or fainting in the setting of
high temperature. Physical examination usually reveals tachycardia, and skin is pale, cool, and
sweaty. Patients may or may not have orthostatic vital signs. An important aspect of heat
syncope is that any alteration in mentation resolves immediately after the event. If there is any
sustained altered mental status, the patient is suffering from heat stroke. Treatment for heat
syncope consists of rest in a cool environment, as well as oral or intravenous fluid replacement.
9. What are the symptoms of heat exhaustion and how is it treated?
Patients with heat exhaustion complain of flu-like symptoms, weakness, thirst, nausea/
vomiting, sweating. Their heart rate may be normal or tachycardic. Body temperature is
usually normal, but will not exceed 40°C (104°F). Patients should be removed from the warm
environment and hydrated. Hydration can occur by either the oral route (if the patient can
tolerate this) or intravenously. The most important aspect of treating heat exhaustion is
ensuring that it does not progress to heat stoke. Remember that a patient’s perception of
temperature does not always correlate with core temperature.
10. What is heat stroke?
Heat stroke is a life-threatening medical emergency. It is characterized by an elevated core
body temperature (.40°C), accompanied by mental status changes and varying degrees of
organ dysfunction. The patient may or may not be sweating. Signs and symptoms may
include confusion, seizures, coma, acute renal failure, respiratory failure, liver failure,
disseminated intravascular coagulation, or ischemic bowel.
11. Describe the two types of heat stroke and how they are differentiated.
n
Exertional heat stroke is usually observed in athletes, laborers, military, or other young
healthy individuals involved in strenuous physical activity who may not be acclimatized to
their environment. The thermoregulatory system functions normally but becomes
overwhelmed.
n
Nonexertional, or classic, heat stroke occurs in individuals who are exposed to excessive
temperatures and who are unable to alter their environment. People that are particularly
vulnerable to this condition include the poor, the elderly, infants, alcoholics, patients with
chronic medical conditions, or patients that do not have access to cooling mechanisms
such as fans or air conditioning.
12. What laboratory abnormalities would be expected in patients with heat illness?
Laboratory abnormalities may include acute renal failure, hemoconcentration, elevated liver
function tests, rhabdomyolysis, hyper/hyponatremia, hyper- or hypokalemia, leukocytosis, and
Chapter 58 HEAT ILLNESS 409
disseminated intravascular coagulation. Renal failure, rhabdomyolysis, and disseminated
intravascular coagulation are more common in victims of exertional heat stroke than in victims
of classic heat stroke.
13. What is the treatment of heat stroke?
Core body temperature should be monitored continuously via rectal thermometer. The patient
should be rapidly cooled, with a goal temperature of ,38.9°C (102°F) within 30 minutes of
presentation to minimize organ damage. You cannot cool too quickly. Evaporative cooling
methods are the safest and may involve continually wetting the patient with tepid water while
the skin is fanned, allowing for continuous airflow over moist skin. Cold water is not
necessary and may induce shivering and vasoconstriction. A cooling blanket may be utilized,
or ice packs applied to the axillae, neck, and groin. Emersion in ice water baths is also an
effective way of cooling patients, although not practical in all settings. Invasive cooling
techniques, such as iced gastric or peritoneal lavage, have been studied but do not have a
clear advantage over evaporative cooling.
Along with rapid cooling, supportive care should be initiated. Intubation may be
necessary if the patient is unable to protect their airway. Hemodynamics and urine output
should be monitored carefully, with intravenous fluids and electrolyte replacement. Although
patients with heat illness are almost uniformly dehydrated, over-resuscitation should be
avoided.
14. Are any medications indicated in the treatment of heat stroke?
Benzodiazepines may be used to control shivering. Antipyretic agents such as acetaminophen
or salicylic acid have not been shown to be beneficial. Dantrolene, which is used to treat
malignant hyperthermia, is not effective in the treatment of heat stroke.
15. What are the risk factors that can lower the threshold for heat stroke?
Risk factors include age (infants, young children, and the elderly), inability to care for oneself,
alcohol abuse, obesity, dehydration, non-acclimatization, and chronic medical conditions and
medications (such as b-blockers) that can limit the ability to respond to changes in
temperature.
16. What is the differential diagnosis for hyperthermia with central nervous
system dysfunction?
n
Acute infection, including sepsis and meningitis
n
Status epilepticus
n
Serotonin syndrome
n
Neuroleptic malignant syndrome
n
Drugs, such as cocaine, alcohol, caffeine, diuretics, psychotropics, and phenothiazines
n
Thyroid storm
n
Stroke
17. What is the mortality rate associated with heat stroke?
Mortality rate varies depending on a number of factors: age, underlying comorbidities, and
most importantly the degree and duration of hyperthermia. In addition, the setting of heat
stroke affects the mortality rate. Mortality rates can exceed 50%. Poor prognostic
indicators include advanced age, hypotension, and respiratory failure requiring intubation.
Aggressive treatment may reduce the mortality, particularly in patients with exertional
heat stroke.
18. What about prevention?
Acclimatization is the key. The process can take a week or more and involves limited activity
during that period of time. Acclimatization allows sweating to increase and proteins to change
to better tolerate heat. It is important to resist the temptation to participate in strenuous
activity early in a heat wave and allow the acclimatization process to take effect.
Chapter 58 HEAT ILLNESS410
KEY POINTS: HEAT ILLNESS
1. Heat stroke is life-threatening and is defined by altered mental status. Heat stroke victims
may or may not be sweating.
2. You cannot cool a patient too quickly.
3. Evaporative cooling is quick, safe, and effective.
BIBLIOGRAPHY
1. Bouchama A, Knochel JP: Heat stroke. N Engl J Med 3346. (25):1978–1988, 2002.
2. Hadad E, Rav-Acha M, Heled Y, et al: Heat stroke: a review of cooling methods. Sports Med 34(8):501–511,
2004.
3. Lugo-Amador NM, Rothenhaus T, Moyer P: Heat-related illness. Emerg Med Clin North Am 22:315–327, 2004.
ACKNOWLEDGMENT
The editors gratefully acknowledge the contributions of David J. Vukich, MD, author of this chapter
in the previous edition.
411
ALTITUDE ILLNESS AND DYSBARISMS
CHAPTER 59
Jeffrey Druck, MD, and Christopher Davis, MD
1. What are the three disease states that comprise high altitude illness?
High altitude illness is comprised of three distinct clinical entities:
n
Acute mountain sickness (AMS)
n
High-altitude pulmonary edema (HAPE)
n
High-altitude cerebral edema (HACE)
2. What are the symptoms of AMS?
AMS is defined as the presence of a headache in the setting of recent ascent to high altitude
with one of the following additional complaints: anorexia, nausea, vomiting, fatigue, weakness,
dizziness, lightheadedness, or difficulty sleeping. It is an entirely clinical definition.
3. How quickly do symptoms of AMS develop? What elevation is the minimum
elevation at which one can see AMS?
Usually, symptoms begin within 6 to 10 hours of ascent. The minimum elevation at which
AMS has been documented is 2000 m (6562 ft).
4. How do I treat AMS?
AMS is usually a self-limited disease that resolves with acclimatization (usually within
1–2 days); the real concern is for further progression to HACE or development of HAPE with
further ascent. Treatment is tailored to the severity of the symptoms and includes descent,
acetazolamide (250 mg twice a day), supplemental oxygen, and dexamethasone.
KEY POINTS: TREATMENT FOR ALL TYPES OF HIGH-ALTITUDE
ILLNESS
1. Descent (best treatment)
2. Supplemental oxygen
3. Hyperbaric therapy
5. What is the number-one risk factor for AMS?
Age. Although controversial, in one study, subjects younger than 25 years were 2.6 times
more likely to develop AMS than those older than 55 years. However, studies on young
children show no increased risk. Additional predisposing factors associated with AMS are as
follows:
n
Rate of ascent
n
Exertion on arrival
n
Elevation attained
n
Previous history of AMS
n
Duration of stay at altitude
n
Cold temperatures
Chapter 59 ALTITUDE ILLNESS AND DYSBARISMS412
A recent study demonstrates that the hyperventilatory capacity (oxygen saturation after
1 minute of hyperventilation) may be directly related to one’s risk of developing AMS.
6. Is there any treatment that will prevent AMS?
The easiest way to prevent AMS is by minimizing risk. Slow ascent, avoidance of sedatives
(alcohol included), and decreased physical activity on arrival minimize risk. Data support using
either acetazolamide at 125 mg twice a day starting the day prior to ascent and continuing for
2 days at maximum altitude, or dexamethasone at 4 mg twice a day for the same time period.
The data on Gingko biloba for the treatment of AMS remain controversial. However, recent
studies show that varying purities in Gingko biloba likely contribute to the variability in
efficacy.
KEY POINTS: PREVENTION FOR ALL TYPES OF HIGH-ALTITUDE
ILLNESS
1. Slow ascent
2. Limitation of exertion
3. Avoidance of sedatives
4. Acetazolamide or dexamethasone
7. What is the definition of HACE?
HACE is a clinical diagnosis defined by a change in consciousness and associated ataxia in the
setting of ascent to altitude. Cerebral edema is often present on computed tomography (CT)
scans, and death results from brain herniation.
8. When does HACE occur?
The onset of HACE usually occurs 3 to 5 days after arrival to elevation.
9. What is the treatment for HACE?
Treatment includes immediate descent, supplemental oxygen, and dexamethasone. If descent
is not an option, hyperbaric therapy (simulating descent) is a possibility; other modalities,
such as diuretics or acetazolamide, are untested and are of unproven benefit.
10. Is there anything that will prevent HACE?
Because HACE is thought to be the end point on the spectrum of altitude illness, prevention
strategies for AMS are the same for HACE.
11. What is HAPE?
HAPE is defined as two of the following symptoms in the setting of a recent gain in altitude:
n
Dyspnea at rest
n
Cough
n
Weakness or decreased exercise tolerance
n
Chest tightness or congestion and two of the following signs:
Crackles or wheezing in at least one lung field
Central cyanosis
Tachypnea
Tachycardia
HAPE is thought to be noncardiogenic pulmonary edema resulting from failure of the alveolar-
capillary barrier. Cold stress and exertion increase pulmonary arterial pressure, which
contributes to an increase in pulmonary edema.
Chapter 59 ALTITUDE ILLNESS AND DYSBARISMS 413
12. When does HAPE occur?
Usually, HAPE occurs within 1 to 3 days of arrival at altitude and is rare beyond 4 days.
13. How do I treat HAPE?
Descent, supplemental oxygen, and hyperbaric therapy are the mainstays of treatment.
Temporizing measures aimed at decreasing pulmonary artery pressures (nifedipine and
expiratory positive airway pressure masks) have been shown to help, but the recovery period
from HAPE is measured in days, so definitive therapy such as descent is highly recommended.
b-agonists that promote alveolar fluid clearance may also be beneficial. Other vasodilators
such as nitric oxide, tadalafil, and sildenafil are currently being researched and show promise.
In contrast with HACE and AMS, dexamethasone has no effect.
14. Is there any preventative therapy for HAPE?
Nifedipine has been shown to decrease the recurrence of HAPE in patients with previous
HAPE. New data suggest acetazolamide does not prevent HAPE, although further studies are
ongoing. In general, the principles designed to decrease the incidence of AMS (slow rate of
ascent, decreased activity at altitude, no sedatives) are also true for HAPE.
15. Do you ever see HAPE, HACE, or AMS at the same time?
HACE is thought to be end-stage AMS, so you do not see both at the same time. HACE
often occurs in association with HAPE, but you can see HAPE without any signs of AMS
or HACE.
16. Which form of altitude illness is most common? Which is most deadly?
The incidence of altitude illnesses depends on the altitude achieved in the group studied:
n
AMS: Incidence, 15% to 70% (most common); mortality rate, 0%
n
HACE: Incidence, 1% to 2%; mortality rate unknown because of usually coexistent HAPE
n
HAPE: Incidence: 1% to 15%; mortality rate, as high as 44% (most deadly)
17. What is dysbarism?
Dysbarism refers to pressure-related diseases but is commonly limited to diseases resulting
from diving injuries (underwater pressure changes). This category includes diseases related
specifically to pressure changes and their physical effects (e.g., middle ear barotrauma
[MEBT], pneumothorax, arterial gas embolism, pneumomediastinum, and barosinusitis) as
well as disease related to bubble formation (e.g., pulmonary decompression sickness, spinal
decompression sickness, and the bends).
18. How much pressure does a diver experience at 33 ft underwater?
Each 33 ft, or 10 m, is equivalent to 1 atmosphere. Because sea level is equivalent to
1 atmosphere, 33 ft underwater is 2 atmospheres, which is equal to 29.4 psi or 1,520 mm Hg.
19. What are the bends?
The bends, also known as caisson’s disease (named after caisson workers, who work in
pressurized underwater chambers), is one of the more common forms of dysbarism. It
occurs when nitrogen comes out of solution and forms bubbles in tissues, causing muscle
and joint pain.
20. When would you see someone with the bends?
People experience the bends when they ascend too rapidly from scuba diving.
21. Why would nitrogen precipitate in tissues?
According to Boyle’s law of gases, pressure is inversely proportional to volume (P
1
V
1
5 P
2
V
2
).
Add into this mixture Henry’s law that states that the amount of gas in solution is directly
proportional to the partial pressure of that gas. Thus, with increased pressure underwater, the
volume of gas decreases, and the amount of gas in solution (dissolved) increases. However,
with rapid ascent, gas will expand and come out of solution, resulting in increased gas bubble
Chapter 59 ALTITUDE ILLNESS AND DYSBARISMS414
size and possible precipitation in tissues. With a slow ascent, the gradual increase in bubble
size and slow change in amount of gas in solution allow the gases to remain dissolved in
circulating blood and expelled through the respiratory system.
22. What is nitrogen narcosis?
As stated previously, the amount of each gas that goes into solution in the blood increases
with increased pressure (or increased depth, because increased depth causes increased
pressure). With nitrogen being the largest component of air, a large amount of nitrogen goes
into solution in the blood, ever increasing with increasing pressure. This high concentration of
nitrogen causes an anesthetic-like effect that causes lack of motor control and inappropriate
behavior, and eventually causes unconsciousness. Nitrogen narcosis usually is seen at depths
of 100 ft or more. To avoid nitrogen narcosis, alternative mixtures containing decreased
nitrogen are recommended for dives greater than 100 ft.
23. What is MEBT?
MEBT occurs when the pressure of the water on the tympanic membrane during descent is
not equalized by the eustachian tube. Usually, a diver will mechanically increase the pressure
in his or her middle ear by forcing air through the eustachian tube to equilibrate the pressure
across the tympanic membrane; if this does not occur, the increased external pressure will
cause pain until rupture of the tympanic membrane eventually occurs, which may cause
severe vertigo.
24. How would one get a pneumothorax with ascent?
If a diver held his or her breath to go underwater to 33 ft (2 atm), the volume in the lungs
would decrease to half the prior volume (1 atm 3 normal lung volume 5 2 atm 3
1
⁄2
normal lung volume). If he or she is scuba diving and replaces that lung volume back to
normal, with ascent, he or she could double the lung volume (2 atm 3 normal lung
volume 5 1 atm 3 2 normal lung volume). If there is nowhere for this additional gas to
escape (i.e., breath holding), the lung may rupture, causing a pneumothorax to develop.
25. What is arterial gas embolism (AGE)?
This condition occurs when expanding gas ruptures an alveolus and the gas is forced into the
pulmonary vasculature. The gas is then distributed through the arterial system, with typical
symptoms of loss of consciousness, apnea, and cardiac arrest. It is the second most common
cause of diving-related deaths.
26. What about the movies that show people bleeding from their eyes when
diving? Does that really happen?
With typical diving masks, an artificial air space is created in front of the eyes. When a diver
descends, this air space is subject to the same gas laws as the diver, with the volume of air in
the mask decreased by one half at 1 atmosphere underwater (effectively 2 atmospheres), one
third at an effective 3 atmospheres, and so forth. This pressure change creates a vacuum
effect in the mask, which can cause petechial hemorrhage, subconjunctival hemorrhage, and
even optic nerve damage, termed facial barotrauma. The usual way divers avoid this problem
is by wearing a mask that encompasses their nose and then equalizing the pressure by
blowing air into their mask.
27. What is decompression sickness (DCS)?
This term that describes the diseases that occur when gas (usually nitrogen) precipitates out
of solution. The earliest form of DCS is the bends, the disease that presents as limb and joint
pain. Prior thought was that the bends resulted from gas precipitation within joints
themselves, but further research has shown that the gas distension occurs along ligaments
and tendon sheaths. Other components of DCS include pulmonary DCS (“the chokes”), skin
DCS (skinny bends), and spinal cord DCS. Type I DCS includes skin and musculoskeletal
symptoms; type II DCS includes all other symptoms.
Chapter 59 ALTITUDE ILLNESS AND DYSBARISMS 415
28. What are the chokes?
The chokes is the common term for pulmonary DCS. Pulmonary DCS manifests as cough,
shortness of breath, and chest pain resulting from massive venous gas embolism, which
enters into the pulmonary artery.
29. What are the skinny bends?
Skinny bends refers to cutaneous DCS, which is the appearance of a diffuse, reticulated,
blotchy rash caused by endothelial damage from bubbles, resulting in blood extravasation. It
can also refer to a syndrome of cutaneous itching that only appears in the artificial
environment of a hyperbaric chamber.
30. What is spinal cord DCS?
Spinal cord DCS is a syndrome characterized by ascending paresthesias and paralysis
resulting from venous outflow obstruction by venous gas emboli in the epidural plexus of the
spinal cord.
31. Is there a central nervous system (CNS) form of DCS?
Yes. It commonly presents with headache, blurred vision, dysarthria, diplopia, and
inappropriate behavior. The exact mechanism of CNS DCS is poorly characterized; there was
some thought that it was caused by venous gas embolism going across a patent foramen
ovale (PFO), but the incidence of PFOs in patients with CNS DCS is equivalent to the general
population.
32. How do you tell the difference between CNS DCS and AGE?
One main point is that loss of consciousness is uncommon with CNS DCS. However, because
both are treated the same way, there is little use in distinguishing between the two.
33. How are dysbarisms treated?
In general, DCS and AGE should be treated with immediate recompression in a hyperbaric
oxygen chamber. The longer the delay to treatment, the higher the morbidity and mortality.
Acute pressure-related injuries (e.g., pneumothorax, pneumomediastinum) should be treated
with standard therapy, whereas tympanic membrane rupture and inner ear disturbances
should be referred to an otolaryngologist. Facial barotrauma victims should be assessed for
more serious injuries, but there usually is no further treatment needed. The best way to treat
dysbaric injuries is to prevent them from occurring in the first place. Some data suggest
immediate oxygen therapy may result in better outcomes.
34. Is there anything that makes a particular person susceptible to DCS?
Although controversial, there are data that increased age is a risk factor for DCS. Also,
inexperience is linked to an increased incidence in DCS.
35. Is there anything that I can do to reduce my risk of DCS?
Slow ascent is the key. There are some data that show a decrease in the incidence of DCS in a
rat model with exercise 20 hours prior to diving, but further research needs to be done. Air
mixtures such as nitrox, a nitrogen and oxygen gas mixture with greater than 21% oxygen, or
heliox, a mixture of helium and oxygen, also show promise.
KEY POINTS: TYPES OF DCS
1. Type I: Skin DCS (skinny bends) and musculoskeletal DCS (the bends)
2. Type II: Pulmonary DCS (the chokes), spinal cord DCS, and CNS DCS
Chapter 59 ALTITUDE ILLNESS AND DYSBARISMS416
BIBLIOGRAPHY
1. Basnyat B, Gertsch JH, Johnson EW, et al: Efficacy of low dose acetazolamide (125 mg BID) for the
prophylaxis of acute mountain sickness: a prospective, double-blind, randomized, placebo controlled trial.
High Alt Med Biol 4:45–52, 2003.
2. Basnyat B, Hargrove J, Holck PS, et al: Acetazolamide fails to decrease pulmonary pressure at high altitude in
partially acclimatized humans. High Alt Med Biol 9:209–216, 2008.
3. Ellsworth AJ, Larson EB, Strickland D: A randomized trial of dexamethasone and acetazolamide for acute
mountain sickness prophylaxis. Am J Med 83:1024–1030, 1987.
4. Gallager SA, Hackett PH: High altitude illness. Emerg Med Clin North Am 22:329–355, 2004.
5. Hayat A, Hussain MM, Aziz S, et al: Hyperventilatory capacity—a predictor of altitude sickness. J Ayub Med
Coll Abbottabad 18:17–20, 2006.
6. Leadbetter G, Keyes LE, Maakestad KM, et al: Gingko biloba does—and does not—prevent acute mountain
sickness. Wilderness Environ Med 20:66–71, 2009.
7. Longphre JM, Denoble JM, Moon RE, et al: First aid normobaric oxygen for the treatment of recreational
diving injuries. Undersea Hyperb Med 34:43–49, 2007.
8. Maggiorini M, Brunner-La Rocca HP, Peth S, et al: Both tadalafil and dexamethasone may reduce the
incidence of high-altitude pulmonary edema. Ann Intern Med 145: 497–506, 2006.
9. Sartori C, Allemann Y, Duplain H, et al: Salmeterol for the prevention of high altitude pulmonary edema.
N Engl J Med 346:1631–1636, 2002.
10. Shockley LW: Scuba diving and dysbarism. In Marx JA, Hockberger RS, Walls RM, et al, editors: Rosen’s
emergency medicine: concepts and clinical practice, ed 5, St. Louis, 2002, Mosby, chapter 137.
11. Wisloff U, Richardson RS, Brubakk AO: Exercise and nitric oxide prevent bubble formation: A novel approach
to the prevention of decompression sickness? J Physiol 553:825–829, 2004.
WEBSITES
Preventing the Bends: www.ntnu.no/gemini/2003-06e/15.htm
417
XIII. NEONATAL AND CHILDHOOD DISORDERS
EVALUATION OF FEVER IN CHILDREN
YOUNGER THAN AGE THREE
CHAPTER 60
Genie E. Roosevelt, MD, MPH
1. What is fever?
Fever is generally defined as a rectal temperature of 38.0°C (100.4°F). Be aware that parents
often consider a fever below the 38.0°C mark, as when parents say, “She had a fever of 99.2°.”
2. How should temperature be measured in infants and young children?
For infants from birth up to 3 months of age, the most reasonable and accurate method is the
rectal temperature. Tympanic temperatures are appropriate in children older than 3 months of
age. Oral temperatures are generally not attempted in young children for obvious logistical
reasons. Axillary temperatures are unreliable and should not be used despite the ease with
which they may be obtained.
3. Is it safe to measure temperatures rectally?
Many parents, and even health care providers, are anxious about doing this. British studies
investigating safety and efficacy demonstrate an extremely low risk of injury.
4. What is a serious bacterial infection (SBI)?
SBI includes:
n
Bacteremia
n
Urinary tract infection (UTI)
n
Bacterial meningitis
n
Pneumonia (established by a focal infiltrate on chest X-ray)
5. Does it matter how much fever the child has?
Hyperpyrexia (temperature of 40.5°C) has been associated with higher rates of SBI (4%) in
patients 3 to 36 months of age. However, any child who appears toxic should be evaluated for
SBI regardless of the temperature.
6. What is meant by toxic appearing?
Toxic children may be pale, lethargic, or limp. They may show evidence of poor perfusion (such
as cyanosis or peripheral vasoconstriction with mottling) or changes in respiratory drive such as
tachypnea or shallow breathing. They may fail to interact with their environment (as evidenced by
poor or absent eye contact, poor feeding, or failure to respond to caregivers or objects in their
view). These children are generally very ill, requiring immediate resuscitation and evaluation.
KEY POINTS: SIGNS OF TOXICITY
1. Lethargy
2. Cyanosis
3. Tachypnea
4. Poor tone
5. Failure to respond to caregivers