1st Article

Question 1

A 36-year-old man with a history of alcohol and substance abuse was admitted to this hospital because of

Answer 1

severe agitation and paranoia

Question 2

Three days before admission, he began drinking alcohol and taking

Answer 2

“bath salts” (psychoactive drugs) intranasally after having had no sleep and minimal oral intake.

Question 3

The night before admission, increasing agitation developed and was associated with

Answer 3

1. apparent auditory and

2. visual hallucinations that people were trying to harm him.

Question 4

On the morning of admission, shortly after snorting more bath salts,

Answer 4

he ran outside unclothed, shouting that someone was trying to strangle him. His girlfriend called the police, who found him running naked in the street.

Question 5

When emergency medical services personnel arrived, they found him restrained by police officers,

Answer 5

1. combative, and
2. confused, with nonsensical,
3. paranoid, and
4. rambling speech.

Question 6

The pulse was

Answer 6

157 beats per minute, with bounding radial pulses, and the respiratory rate was 24 breaths per minute.

Question 7

The pupils were

Answer 7

1. 5 mm in diameter.
2. The skin was flushed, warm, and diaphoretic.
3. A capillary glucose level was 268 mg per deciliter (14.9 mmol per liter).

Question 8

Soft restraints were applied, and

Answer 8

oxygen was administered through a nonrebreather face mask. The patient was transported to the emergency department at this hospital.

Question 9

En route, he suddenly became quiet, and a

Answer 9

seizure was suspected.

Question 10

The administration of

Answer 10

midazolam was attempted, but the patient pulled out the intravenous catheter.

Question 11

On arrival, the patient was unable

Answer 11

to communicate.

Question 12

His history was obtained from his girlfriend. He had a history of

Answer 12

1. depression,
2. alcohol abuse, and
3. drug abuse (including heroin, cocaine, and prescription opiates)

Question 13

His only medication was

Answer 13

fluoxetine, which he reportedly had not taken for 2 weeks.

Question 14

He was allergic to

Answer 14

shellfish and had no known allergies to medications.

Question 15

He smoked

Answer 15

cigarettes. He lived with his girlfriend and had recently lost his job at a service station.

Question 16

He had a family history of

Answer 16

1. hypertension,
2. coronary artery disease, and
3. diabetes mellitus.

Question 17

On examination, the patient was

Answer 17

1. agitated,
2. flailing his arms and legs,
3. jerking his head, and
4. making loud incomprehensible sounds.
5. He was unable to cooperate during the examination and required restraining by several security officers.

Question 18

The temperature was

Answer 18

1. 37.0°C (normal temp)
2. the blood pressure 157/67 mm Hg,
3. the pulse 173 beats per minute,
4. the respiratory rate 28 breaths per minute, and
5. the oxygen saturation 97% while he was breathing ambient air.

Question 19

The skin was

Answer 19

diaphoretic.

Question 20

The pupils were

Answer 20

equal and reactive to light;

Question 21

the gaze was deviated

Answer 21

upward, with slow, horizontal ocular movements.

Question 22

The patient’s speech was

Answer 22

1. rapid and mostly unintelligible,
2. but he made references to attacking and being attacked by animals, people, and monsters.
3. The remainder of the examination was normal.

Question 23

The prothrombin time, prothrombin-time international normalized ratio, and results of liver-function tests were

Answer 23

normal, as were blood levels of calcium, total protein, albumin, and globulin; other test results are shown in Table 1.

Question 24

Urinalysis revealed

Answer 24

clear, yellow urine with a specific gravity greater than 1.030, a pH of 5.5, 2+ occult blood, 1+ albumin, and trace ketones by dipstick.

Question 25

There were

Answer 25

1. 3 to 5 red cells,
2. 10 to 20 white cells,
3. few squamous cells, and
4. very few renal tubular cells per high-power field and
5. few bacteria and
6. 3 to 5 hyaline and granular casts per low-power field; 7. mucin was present.

Question 26

Urinalysis was otherwise

Answer 26

normal. The urine creatinine level was 3.50 mg per milliliter.

Question 27

The patient was restrained, and

Answer 27

midazolam was administered intravenously, followed by lorazepam, but his condition did not improve.

Question 28

Etomidate and rocuronium were administered, the trachea was .

Answer 28

intubated, and mechanical ventilation was begun, followed by sedation with propofol

Question 29

A urinary catheter and an esophagogastric tube were inserted. A chest radiograph showed

Answer 29

1. low lung volumes and

2. the correct placement of the endotracheal and gastric tubes;

Question 30

changes consistent with pulmonary edema or pneumothorax were

Answer 30

not observed.

Question 31

A computed tomographic scan of the head, obtained without the administration of contrast material, showed

Answer 31

no acute intracranial hemorrhage, infarction, or mass lesion.

Question 32

An electrocardiogram showed

Answer 32

1. sinus rhythm at a rate of 113 beats per minute, with

2. inverted T waves in the inferior leads and nonspecific T-wave abnormalities in the lateral leads.

Question 33

what were administrated to the pt after EKG?

Answer 33

1. Fomepizole,
2. sodium thiosulfate,
3. sodium bicarbonate,
4. normal saline, and
5. potassium chloride were administered intravenously, and

Question 34

the patient was admitted to the

Answer 34

1. intensive care unit.
2. The pulse fell to 92 beats per minute, and
3. 290 ml of urine was excreted.

Question 35

This patient arrived in the emergency department with

Answer 35

1. agitation,
2. delirium,
3. abnormal vital signs, and reports that he had taken a toxic substance.

Question 36

The first priority in the emergency department is to ensure the safety of the patient and caregivers. It was necessary to immediately

Answer 36

restrain this patient and sedate him, because he was at risk of harming himself and the staff.

Question 37

The initial evaluation must include a search for

Answer 37

1. any toxin on the patient’s body and clothing or

2. any exhaled or excreted toxin that could harm the emergency department staff.

Question 38

He did not have any

Answer 38

1. visible solid or liquid substances on his body or

2. any unusual odors.

Question 39

Initial Management Physical restraints on an agitated patient may cause injury to the caregiver who is applying the restraints, as well as

Answer 39

1. skin injury and

2. rhabdomyolysis in the patient.

Question 40

In view of the tachycardia and hypertension that were present on prehospital evaluation, it was appropriate to sedate this patient with

Answer 40

a parenteral benzodiazepine, which usually has a mild effect on the blood pressure; any decrease in respiratory effort can usually be managed with supplemental oxygen and bag-mask ventilation.

Question 41

In addition, benzodiazepines are useful for

Answer 41

seizure control and for treatment of patients who have taken

1. sympathomimetic drugs or
2. who have ethanol withdrawal.

Question 42

If moderate doses of a benzodiazepine do not control the agitation, the

Answer 42

airway should be secured through endotracheal intubation, as was done in this case, to allow for the administration of higher doses of sedatives that could cause respiratory depression and the loss of protective mechanisms in the airway.

Question 43

The initial history, as described by the patient’s girlfriend, indicated that the patient had taken

Answer 43

1. a toxic substance, and this report is consistent with his presentation with agitated delirium and
2. elevated heart rate and blood pressure.

Question 44

However, it is important not to dismiss other causes; at this point in the evaluation,

Answer 44

1. infectious and

2. psychiatric causes were still possible.

Question 45

what symptom of the pt led to consider infectious cause?

Answer 45

the pt’s altered mental status

Question 46

Infectious Causes–> Central nervous system infections need to be considered and treated urgently in the emergency department. Given this patient’s altered mental status, we need to consider

Answer 46

1. meningitis and

2. encephalitis.

Question 47

In a young, healthy patient, it is unlikely that altered mental status caused by

Answer 47

1. pneumonia or

2. pyelonephritis would be manifested by altered mental status,

Question 48

but what would be a concern for altered mental status?

Answer 48

pulmonary aspiration caused by a toxic ingestion and vomiting would be a concern.

Question 49

in this case based on what the infection could be ruled out?

Answer 49

1. urinalysis and
2. chest radiography revealed no evidence of infection and
3. the results of brain imaging were normal.

Question 50

Many patients who present to the emergency department have a

Answer 50

history of drug abuse, but many also have a history of psychiatric disease.

Question 51

This patient’s agitated delirium was more likely to have a

Answer 51

1. toxic or

2. metabolic cause than a psychiatric one.

Question 52

based on what raises concern about underlying psychosis?

Answer 52

However, the history, reported by the girlfriend, of 1. increasing paranoia and
2. auditory and visual hallucinations raises concern about underlying psychoses.

Question 53

Psychiatric assessments would need to wait until

Answer 53

the delirium had resolved.

Question 54

It frequently takes hours or days for the results of toxicologic studies to become available, and thus emergency department clinicians must

Answer 54

determine the initial treatment on the basis of the early clinical signs and symptoms that were observed after a toxic substance was taken.

Question 55

Clinical signs and symptoms are organized into toxidromes according to

Answer 55

drug class.2 In evaluating this patient’s condition, I have tried to match his clinical presentation to the most likely toxidrome.

Question 56

Patients who have taken amphetamines or cocaine commonly present with

Answer 56

1. tachycardia,
2. hypertension,
3. anxiety,
4. psychomotor agitation,
5. diaphoresis, and
6. mydriasis, and such patients may have psychotic, self-destructive behavior.
7. Seizures can occur.

Question 57

This patient’s presentation is consistent with the use of a

Answer 57

sympathomimetic drug.

Question 58

Sedative or ethanol withdrawal is characterized by

Answer 58

agitated delirium and features associated with the use of sympathomimetic agents.

Question 59

Marked tremors are usually seen in patients with

Answer 59

1. sedative or
2. ethanol withdrawal, and
3. seizures are common early in the withdrawal process.

Question 60

In patients who have taken benzodiazepines, seizures can be

Answer 60

severe and result in status epilepticus.

Question 61

Visual hallucinations are the hallmark of

Answer 61

severe ethanol withdrawal (delirium tremens).

Question 62

This patient had many features of a withdrawal-related toxidrome, but nothing

Answer 62

1. in his history suggested he had sedative or
2. ethanol withdrawal, and
3. there were no marked tremors.

Question 63

Anticholinergic agents (e.g., atropine and its congeners and cyclic antidepressants) can cause

Answer 63

1. altered mental status,
2. tachycardia,
3. mydriasis,
4. acute urinary retention,
5. decreased bowel sounds, and
6. fever but do not cause diaphoresis.

Question 64

Patients who have taken an overdose of anticholinergic agents are said to be

Answer 64

“dry as a bone, blind as a bat, red as a beet, hot as an oven, and mad as a hatter.”

Question 65

This patient had altered mental status but did not show the other signs of

Answer 65

anticholinergic-drug abuse.

Question 66

The Serotonin Syndrome and the Neuroleptic Malignant Syndrome –>
Patients who have taken large doses of serotonergic medications can present with

Answer 66

1. agitated delirium,
2. autonomic dysfunction (fever, tachycardia, hypertension, and diaphoresis), and
3. neuromuscular hyperactivity.
   - -> This clinical presentation is known as the serotonin syndrome.

Question 67

The neuroleptic malignant syndrome is characterized by

Answer 67

1. fever,
2. muscular rigidity,
3. altered mental status, and
4. autonomic instability in patients who recently have begun taking a prescribed neuroleptic medication or have had a dosage increase.

Question 68

This patient presented with many of the characteristics of

Answer 68

1. the serotonin syndrome and
2. the neuroleptic malignant syndrome,
3. but he does not have a clear recent history of taking serotonergic or neuroleptic substances.

Question 69

However, drugs obtained on the street frequently

contain

Answer 69

unexpected substances, and so these diagnoses cannot be dismissed.

Question 70

Anion-Gap Acidosis

This patient presented with severe anion-gap acidosis, which can be caused by

Answer 70

many substances.

Question 71

During the initial evaluation, the clinical staff focused on two toxic substances that the patient may have taken,

Answer 71

1. cyanide and

2. toxic alcohol (methanol or ethylene glycol).

Question 72

Since there are effective antidotes for these substances, and since the patient’s history was

Answer 72

unclear, the team decided to presumptively treat him for both substances.

Question 73

The team administered sodium thiosulfate, which reacts with

Answer 73

cyanide to form the nontoxic thiocyanate,

Question 74

and fomepizole (4-methylpyrazole), an alcohol dehydrogenase inhibitor that limits the

Answer 74

toxic effects of methanol and ethylene glycol.

Question 75

Bath Salts –>

The patient’s girlfriend indicated that the patient had recently taken

Answer 75

bath salts by nasal insufflation.

Question 76

These bath salts are not sodium chloride bath salts or Epsom salts; rather, they are synthetic derivatives of

Answer 76

cathinone, a sympathomimetic chemical found in the leaves of the khat plant (Catha edulis).

Question 77

The use of bath salts is associated with

Answer 77

1. sympathomimetic activity and

2. psychotic behavior (e.g., paranoia, hallucinations, and self destructive and aggressive behavior).

Question 78

The diagnostic test for bath salt was screening of the

Answer 78

blood and urine for toxins.

Question 79

The use of a synthetic cathinone (bath salts), causing

Answer 79

1. a sympathomimetic toxidrome with psychotic features, 2. an acute lactic acidosis, and
2. rhabdomyolysis with renal failure.

Question 80

The laboratory tests detected

Answer 80

1. lorazepam,
2. fluoxetine,
3. norfluoxetine, and
4. methcathinone in the patient’s blood.

Question 81

The blood tests were negative for common stimulants, such as

Answer 81

1. amphetamine,
2. methamphetamine,
3. methylenedioxymethamphetamine (MDMA, or “ecstasy”), and
4. cocaine.

Question 82

Class-specific immunoassays of the urine were positive for

Answer 82

1. amphetamines and

2. benzodiazepines and

Question 83

negative for

Answer 83

1. barbiturates,
2. cocaine metabolites,
3. opiates, phencyclidine, and
4. cannabinoids.

Question 84

The term “bath salts” refers to a diverse, expanding group of synthetic designer drugs belonging to the

Answer 84

cathinone class of sympathomimetic amines.3

Question 85

Cathinones are closely related to other sympathomimetic amines, such as

Answer 85

amphetamines and ephedrine, differing only at the β-carbon of the propyl side chain (Fig. 1A). At the β-carbon position, an absence of substitution is representative of amphetamines, the presence of a ketone group (known as β-keto) is characteristic of a cathinone, and the presence of a hydroxyl group is characteristic
of ephedrine.

Question 86

Methcathinone (ephedrone), which was first synthesized in 1928, is the original designer drug derived

Answer 86

from cathinone.

Question 87

In our laboratory, methcathinone is detected as part of our routine screening for toxins; we use

Answer 87

liquid chromatography in combination with photodiode-array detection.4

Question 88

This process uses both

Answer 88

chromatographic retention time and data from various wavelengths in the ultraviolet spectrum to identify unknown chromatographic peaks in a patient’s blood sample.

Question 89

The conjugation of the β-keto group with the phenyl moiety gives cathinones a distinctly richer ultraviolet spectrum than that of either

Answer 89

methamphetamine or ephedrine (Fig. 1A). The addition or removal of alkyl groups at the carbon or nitrogen atoms of the propyl side chain does not substantially alter the ultraviolet spectrum.5

Question 90

However, the addition of alkyl or alkoxy-type groups directly to the phenyl ring notably changes

Answer 90

the ultraviolet spectrum of the resulting compound; such a change occurs in MDMA and the designer cathinones methylone and mephedrone (Fig. 1B). This patient’s blood sample had a large chromatographic peak at 2.34 minutes, matching the retention time of authentic standards of methcathinone and mephedrone.

Question 91

The ultraviolet spectrum of the substance in the blood (Fig. 1D) matched that of

Answer 91

methcathinone but not that of mephedrone.

Question 92

This patient’s most likely source of methcathinone was

Answer 92

bath salts.

Question 93

An alternative source results from

Answer 93

the metabolism of N,N-dimethylcathinone (Fig. 1C), another cathinone that is known to be abused.

Question 94

We ruled out the latter source (N,N-dimethylcathinone) because

Answer 94

neither the blood sample nor the urine sample contained methylephedrine, the major metabolite of N,N-dimethylcathinone.6

Question 95

It is possible that the laboratory misidentified as

Answer 95

methcathinone another synthetic cathinone that did not undergo phenyl-ring substitution.

Question 96

The addition of alkyl groups at the carbon or nitrogen atoms of the propyl side chain (Fig. 1C) produces

Answer 96

cathinones with an ultraviolet spectrum very similar to that of methcathinone.5 If such a cathinone also had the same chromatographic retention time as methcathinone, it would be easily misidentified as methcathinone.

Question 97

Of the 34 designer cathinones listed by Kelly,3 12 are likely to have

Answer 97

ultraviolet spectra that would cause them to be mistaken for methcathinone.

Question 98

Tandem mass spectrometry can differentiate between

Answer 98

methcathinone and methcathinone look-alikes but is not available 24 hours a day.

Question 99

The positive result on the urine test for amphetamines is also directly attributable to the use of

Answer 99

methcathinone.

Question 100

When we assayed standard d,l-methcathinone solutions using

Answer 100

urinary amphetamine reagents, we found that methcathinone concentrations of 80,000 ng per milliliter and higher caused a positive test result for amphetamines (a methamphetamine solution at a concentration of 1000 ng per milliliter is used to calibrate the assay).

Question 101

This cross-reactivity is understandable given the similarity in

Answer 101

structure of methcathinone and methamphetamine (Fig. 1A), the target analyte in the urine test for amphetamines.

Question 102

The methcathinone metabolite ephedrine probably also contributed to the

Answer 102

observation of immunoreactive amphetamines in the patient’s urine.

Question 103

We concluded that methcathinone is the major finding in the patient’s blood sample that is indicative of the use of

Answer 103

bath salts.

Question 104

We also concluded that methcathinone cross-reacted in this hospital’s KIMS (kinetic interaction of microparticles in solution)

Answer 104

urine immunoassay for amphetamines, contributing to a false positive result.

Question 105

When this patient presented to the emergency department, he showed

Answer 105

1. marked confusion,
2. paranoia,
3. agitation, and
4. autonomic dysfunction and required restraining by security officers, physical restraints, the administration of benzodiazepines, and eventually intubation with mechanical ventilation.

Question 106

The diagnosis of cathinone-induced delirium can be a challenge because

Answer 106

most patients are unable to provide a reliable history at the time of presentation, and the routine drug screens that are performed in most hospitals with the use of immunoassays do not readily detect these compounds.

If an acquaintance of the patient provides a patient history of recent bath salt use, as in this
case, specific testing can be requested, but the results may not be received in time to inform immediate treatment.

Question 107

As in this case, the use of synthetic cathinones often leads to a

Answer 107

false positive screening for amphetamines.

Question 108

Gas or liquid chromatography with mass spectrometry is the standard method for the detection of

Answer 108

cathinones, but this method is of limited clinical value because results can be delayed, and thus it is necessary for caregivers to recognize the clinical toxidrome and manage it appropriately.

Question 109

The clinical presentation of patients with cathinone-induced delirium is similar to the presentation of patients who have taken

Answer 109

sympathomimetic agents and consists of the acute onset of altered mental status, agitated behavior, and autonomic dysfunction, as well as severely violent behavior (similar to the behavior observed with phencyclidine-induced or methamphetamine-induced psychosis).

Question 110

In this patient, increasingly erratic behavior developed along with

Answer 110

1. paranoia (including delusions of persecution),
2. aggressive and violent psychomotor activity requiring physical restraints,
3. tachycardia, and
4. increased blood pressure.

Question 111

The core triad of symptoms

Answer 111

(sudden development of altered mental status, agitated behavior, and autonomic dysfunction) was first described by Bell in 1849 in a study of psychiatric patients.7

Question 112

Over the years, the syndrome consisting of these three symptoms has been referred to by many other names

Answer 112

(e.g., Bell’s mania, acute exhaustive mania, delirious mania, lethal catatonia, agitated delirium, and excited delirium), but it is most accurately categorized as a subset of excitable malignant catatonia.7,8

Question 113

Management of Cathinone-Induced Delirium Once the diagnosis of cathinone-induced delirium has been made or is suspected, the focus should quickly turn to controlling the patient’s

Answer 113

agitated behavior in order to reduce the need for physical struggle with security personnel or physical restraints that may exacerbate injury, hyperthermia, and metabolic acidosis.

Question 114

In patients with cathinone-induced delirium, as in those with malignant catatonia, initial sedation should be achieved with the use of

Answer 114

γ-aminobutyric acid type A (GABAA) agonists such as

1. benzodiazepines or
2. propofol.

Question 115

To minimize or prevent the worsening pyrexia and autonomic instability that occurs with the use of dopamine antagonists in such patients, an agent such as

Answer 115

intravenous haloperidol should be administered judiciously and only after therapy with GABAA agonists is initiated.

Question 116

Monotherapy with dopamine antagonists should be avoided because it may exacerbate the

Answer 116

catecholamine surge and hyperthermia that often occur in patients with cathinone-induced delirium and thus cause the development of the malignant catatonia that is characteristic of the neuroleptic malignant syndrome.

Question 117

On presentation, this patient was given

Answer 117

1. midazolam and lorazepam and had a limited response, and he was subsequently intubated and sedated with
2. propofol for the purpose of further diagnostic evaluation and management.

Question 118

After the patient’s agitation is under control, attention is turned to minimizing or addressing such medical complications as

Answer 118

1. metabolic acidosis,
2. rhabdomyolysis,
3. hyperthermia, and
4. multisystem failure.

Question 119

This patient received aggressive supportive care, including the administration of

Answer 119

1. intravenous fluids,
2. sodium thiosulfate for possible cyanide poisoning,
3. fomepizole for the possible ingestion of ethylene glycol or methanol, and
4. sodium bicarbonate (by continuous infusion) for metabolic acidosis.

Question 120

Once medical stability has been achieved, then the focus should be on

Answer 120

reversing the neurotransmitter dysregulation induced by synthetic cathinones.

Question 121

One of the challenges in treating cathinone-induced delirium is that there are

Answer 121

multiple synthetic cathinones available and each one has a different receptor profile on the serotonergic, dopaminergic, and noradrenergic systems (Fig. 2).

Question 122

Methcathinone, the substance present in this case, has particularly strong effects on the

Answer 122

dopaminergic and noradrenergic systems, as does methamphetamine;

Question 123

however, methcathinone has a much weaker effect on the serotonergic system than does

Answer 123

methamphetamine.3

Question 124

The treatment strategy after the patient was transferred to the intensive care unit took into account the pathophysiology of

Answer 124

cathinone-induced delirium.

Question 125

The administration of midazolam and propofol was quickly stopped, and

Answer 125

dexmedetomidine, an α2-adrenergic agonist that can ameliorate excess noradrenergic activity, was begun.

Question 126

Low-dose haloperidol administered to the pt as a continuous infusion to treat excess

Answer 126

mesolimbic dopaminergic transmission was also initiated.10

Question 127

To avoid administering a dopamine antagonist alone after dexmedetomidine had been discontinued,

Answer 127

phenobarbital was administered because it targets GABAA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), and kainate receptors and ultimately reduces neuroexcitability.

Question 128

The administration of levocarnitine, which facilitates the transport of long-chain free fatty acids across the mitochondrial membrane and thus enhances

Answer 128

antioxidative protection, was also initiated.11

Question 129

On arrival at the intensive care unit, the patient was given

Answer 129

1. propofol and

2. midazolam to maintain adequate sedation.

Question 130

On the second day, he was transitioned from propofol and midazolam to

Answer 130

dexmedetomidine and haloperidol administered intravenously by continuous infusion.

Question 131

On the third day, he was extubated but became agitated and had

Answer 131

copious oral secretions that necessitated reintubation and resedation with intravenous propofol and haloperidol by continuous infusion.

Question 132

On the fourth day, the administration of

Answer 132

phenobarbital was begun. The patient was weaned off haloperidol and propofol, and on the seventh day, he was successfully extubated. By the ninth day, he was completely weaned off phenobarbital and had returned to his baseline mental status.

Question 133

The lactic acidosis resolved by

Answer 133

the second day.

Question 134

Acute renal failure developed owing to a combination of

Answer 134

acute tubular necrosis and rhabdomyolysis;

Question 135

the peak creatine kinase level was

Answer 135

14,965 U (high) per liter, on the third day.

Question 136

The plasma creatinine level peaked at 6.0 mg per deciliter (530 μmol per liter) on the third day, but

Answer 136

the patient maintained sufficient urine output that renal-replacement therapy was not required.

Question 137

The rhabdomyolysis was treated with fluids. Acute liver injury also

Answer 137

developed;

Question 138

aspartate aminotransferase and alanine aminotransferase levels

Answer 138

peaked on the third day at 1937 U per liter and 2309 U per liter, respectively, but these levels returned to normal with supportive care.

Question 139

A ventilator-associated pneumonia due to methicillin-sensitive Staphylococcus aureus developed and was treated with

Answer 139

vancomycin and cefepime for 8 days.

Question 140

On the seventh day, hypertension developed and required treatment with

Answer 140

intravenous nitroglycerin.

Question 141

The blood pressure was controlled with

Answer 141

1. oral labetalol,
2. nifedipine, and
3. clonidine.