1
Q
A 36-year-old man with a history of alcohol and substance abuse was admitted to this hospital because of
A
severe agitation and paranoia
2
Q
Three days before admission, he began drinking alcohol and taking
A
“bath salts” (psychoactive drugs) intranasally after having had no sleep and minimal oral intake.
3
Q
The night before admission, increasing agitation developed and was associated with
A
- apparent auditory and
2. visual hallucinations that people were trying to harm him.
4
Q
On the morning of admission, shortly after snorting more bath salts,
A
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.
5
Q
When emergency medical services personnel arrived, they found him restrained by police officers,
A
- combative, and
- confused, with nonsensical,
- paranoid, and
- rambling speech.
6
Q
The pulse was
A
157 beats per minute, with bounding radial pulses, and the respiratory rate was 24 breaths per minute.
7
Q
The pupils were
A
- 5 mm in diameter.
- The skin was flushed, warm, and diaphoretic.
- A capillary glucose level was 268 mg per deciliter (14.9 mmol per liter).
8
Q
Soft restraints were applied, and
A
oxygen was administered through a nonrebreather face mask. The patient was transported to the emergency department at this hospital.
9
Q
En route, he suddenly became quiet, and a
A
seizure was suspected.
10
Q
The administration of
A
midazolam was attempted, but the patient pulled out the intravenous catheter.
11
Q
On arrival, the patient was unable
A
to communicate.
12
Q
His history was obtained from his girlfriend. He had a history of
A
- depression,
- alcohol abuse, and
- drug abuse (including heroin, cocaine, and prescription opiates)
13
Q
His only medication was
A
fluoxetine, which he reportedly had not taken for 2 weeks.
14
Q
He was allergic to
A
shellfish and had no known allergies to medications.
15
Q
He smoked
A
cigarettes. He lived with his girlfriend and had recently lost his job at a service station.
16
Q
He had a family history of
A
- hypertension,
- coronary artery disease, and
- diabetes mellitus.
17
Q
On examination, the patient was
A
- agitated,
- flailing his arms and legs,
- jerking his head, and
- making loud incomprehensible sounds.
- He was unable to cooperate during the examination and required restraining by several security officers.
18
Q
The temperature was
A
- 37.0°C (normal temp)
- the blood pressure 157/67 mm Hg,
- the pulse 173 beats per minute,
- the respiratory rate 28 breaths per minute, and
- the oxygen saturation 97% while he was breathing ambient air.
19
Q
The skin was
A
diaphoretic.
20
Q
The pupils were
A
equal and reactive to light;
21
Q
the gaze was deviated
A
upward, with slow, horizontal ocular movements.
22
Q
The patient’s speech was
A
- rapid and mostly unintelligible,
- but he made references to attacking and being attacked by animals, people, and monsters.
- The remainder of the examination was normal.
23
Q
The prothrombin time, prothrombin-time international normalized ratio, and results of liver-function tests were
A
normal, as were blood levels of calcium, total protein, albumin, and globulin; other test results are shown in Table 1.
24
Q
Urinalysis revealed
A
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.
25
There were
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.
26
Urinalysis was otherwise
normal. The urine creatinine level was 3.50 mg per milliliter.
27
The patient was restrained, and
midazolam was administered intravenously, followed by lorazepam, but his condition did not improve.
28
Etomidate and rocuronium were administered, the trachea was .
intubated, and mechanical ventilation was begun, followed by sedation with propofol
29
A urinary catheter and an esophagogastric tube were inserted. A chest radiograph showed
1. low lung volumes and
| 2. the correct placement of the endotracheal and gastric tubes;
30
changes consistent with pulmonary edema or pneumothorax were
not observed.
31
A computed tomographic scan of the head, obtained without the administration of contrast material, showed
no acute intracranial hemorrhage, infarction, or mass lesion.
32
An electrocardiogram showed
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.
33
what were administrated to the pt after EKG?
1. Fomepizole,
2. sodium thiosulfate,
3. sodium bicarbonate,
4. normal saline, and
5. potassium chloride were administered intravenously, and
34
the patient was admitted to the
1. intensive care unit.
2. The pulse fell to 92 beats per minute, and
3. 290 ml of urine was excreted.
35
This patient arrived in the emergency department with
1. agitation,
2. delirium,
3. abnormal vital signs, and reports that he had taken a toxic substance.
36
The first priority in the emergency department is to ensure the safety of the patient and caregivers. It was necessary to immediately
restrain this patient and sedate him, because he was at risk of harming himself and the staff.
37
The initial evaluation must include a search for
1. any toxin on the patient’s body and clothing or
| 2. any exhaled or excreted toxin that could harm the emergency department staff.
38
He did not have any
1. visible solid or liquid substances on his body or
| 2. any unusual odors.
39
Initial Management Physical restraints on an agitated patient may cause injury to the caregiver who is applying the restraints, as well as
1. skin injury and
| 2. rhabdomyolysis in the patient.
40
In view of the tachycardia and hypertension that were present on prehospital evaluation, it was appropriate to sedate this patient with
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.
41
In addition, benzodiazepines are useful for
seizure control and for treatment of patients who have taken
1. sympathomimetic drugs or
2. who have ethanol withdrawal.
42
If moderate doses of a benzodiazepine do not control the agitation, the
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.
43
The initial history, as described by the patient’s girlfriend, indicated that the patient had taken
1. a toxic substance, and this report is consistent with his presentation with agitated delirium and
2. elevated heart rate and blood pressure.
44
However, it is important not to dismiss other causes; at this point in the evaluation,
1. infectious and
| 2. psychiatric causes were still possible.
45
what symptom of the pt led to consider infectious cause?
the pt's altered mental status
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
1. meningitis and
| 2. encephalitis.
47
In a young, healthy patient, it is unlikely that altered mental status caused by
1. pneumonia or
| 2. pyelonephritis would be manifested by altered mental status,
48
but what would be a concern for altered mental status?
pulmonary aspiration caused by a toxic ingestion and vomiting would be a concern.
49
in this case based on what the infection could be ruled out?
1. urinalysis and
2. chest radiography revealed no evidence of infection and
3. the results of brain imaging were normal.
50
Many patients who present to the emergency department have a
history of drug abuse, but many also have a history of psychiatric disease.
51
This patient’s agitated delirium was more likely to have a
1. toxic or
| 2. metabolic cause than a psychiatric one.
52
based on what raises concern about underlying psychosis?
However, the history, reported by the girlfriend, of 1. increasing paranoia and
2. auditory and visual hallucinations raises concern about underlying psychoses.
53
Psychiatric assessments would need to wait until
the delirium had resolved.
54
It frequently takes hours or days for the results of toxicologic studies to become available, and thus emergency department clinicians must
determine the initial treatment on the basis of the early clinical signs and symptoms that were observed after a toxic substance was taken.
55
Clinical signs and symptoms are organized into toxidromes according to
drug class.2 In evaluating this patient’s condition, I have tried to match his clinical presentation to the most likely toxidrome.
56
Patients who have taken amphetamines or cocaine commonly present with
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.
57
This patient’s presentation is consistent with the use of a
sympathomimetic drug.
58
Sedative or ethanol withdrawal is characterized by
agitated delirium and features associated with the use of sympathomimetic agents.
59
Marked tremors are usually seen in patients with
1. sedative or
2. ethanol withdrawal, and
3. seizures are common early in the withdrawal process.
60
In patients who have taken benzodiazepines, seizures can be
severe and result in status epilepticus.
61
Visual hallucinations are the hallmark of
severe ethanol withdrawal (delirium tremens).
62
This patient had many features of a withdrawal-related toxidrome, but nothing
1. in his history suggested he had sedative or
2. ethanol withdrawal, and
3. there were no marked tremors.
63
Anticholinergic agents (e.g., atropine and its congeners and cyclic antidepressants) can cause
1. altered mental status,
2. tachycardia,
3. mydriasis,
4. acute urinary retention,
5. decreased bowel sounds, and
6. fever but do not cause diaphoresis.
64
Patients who have taken an overdose of anticholinergic agents are said to be
“dry as a bone, blind as a bat, red as a beet, hot as an oven, and mad as a hatter.”
65
This patient had altered mental status but did not show the other signs of
anticholinergic-drug abuse.
66
The Serotonin Syndrome and the Neuroleptic Malignant Syndrome -->
Patients who have taken large doses of serotonergic medications can present with
1. agitated delirium,
2. autonomic dysfunction (fever, tachycardia, hypertension, and diaphoresis), and
3. neuromuscular hyperactivity.
- -> This clinical presentation is known as the serotonin syndrome.
67
The neuroleptic malignant syndrome is characterized by
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.
68
This patient presented with many of the characteristics of
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.
69
However, drugs obtained on the street frequently
| contain
unexpected substances, and so these diagnoses cannot be dismissed.
70
Anion-Gap Acidosis
| This patient presented with severe anion-gap acidosis, which can be caused by
many substances.
71
During the initial evaluation, the clinical staff focused on two toxic substances that the patient may have taken,
1. cyanide and
| 2. toxic alcohol (methanol or ethylene glycol).
72
Since there are effective antidotes for these substances, and since the patient’s history was
unclear, the team decided to presumptively treat him for both substances.
73
The team administered sodium thiosulfate, which reacts with
cyanide to form the nontoxic thiocyanate,
74
and fomepizole (4-methylpyrazole), an alcohol dehydrogenase inhibitor that limits the
toxic effects of methanol and ethylene glycol.
75
Bath Salts -->
| The patient’s girlfriend indicated that the patient had recently taken
bath salts by nasal insufflation.
76
These bath salts are not sodium chloride bath salts or Epsom salts; rather, they are synthetic derivatives of
cathinone, a sympathomimetic chemical found in the leaves of the khat plant (Catha edulis).
77
The use of bath salts is associated with
1. sympathomimetic activity and
| 2. psychotic behavior (e.g., paranoia, hallucinations, and self destructive and aggressive behavior).
78
The diagnostic test for bath salt was screening of the
blood and urine for toxins.
79
The use of a synthetic cathinone (bath salts), causing
1. a sympathomimetic toxidrome with psychotic features, 2. an acute lactic acidosis, and
3. rhabdomyolysis with renal failure.
80
The laboratory tests detected
1. lorazepam,
2. fluoxetine,
3. norfluoxetine, and
4. methcathinone in the patient’s blood.
81
The blood tests were negative for common stimulants, such as
1. amphetamine,
2. methamphetamine,
3. methylenedioxymethamphetamine (MDMA, or “ecstasy”), and
4. cocaine.
82
Class-specific immunoassays of the urine were positive for
1. amphetamines and
| 2. benzodiazepines and
83
negative for
1. barbiturates,
2. cocaine metabolites,
3. opiates, phencyclidine, and
4. cannabinoids.
84
The term “bath salts” refers to a diverse, expanding group of synthetic designer drugs belonging to the
cathinone class of sympathomimetic amines.3
85
Cathinones are closely related to other sympathomimetic amines, such as
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.
86
Methcathinone (ephedrone), which was first synthesized in 1928, is the original designer drug derived
from cathinone.
87
In our laboratory, methcathinone is detected as part of our routine screening for toxins; we use
liquid chromatography in combination with photodiode-array detection.4
88
This process uses both
chromatographic retention time and data from various wavelengths in the ultraviolet spectrum to identify unknown chromatographic peaks in a patient’s blood sample.
89
The conjugation of the β-keto group with the phenyl moiety gives cathinones a distinctly richer ultraviolet spectrum than that of either
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
90
However, the addition of alkyl or alkoxy-type groups directly to the phenyl ring notably changes
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.
91
The ultraviolet spectrum of the substance in the blood (Fig. 1D) matched that of
methcathinone but not that of mephedrone.
92
This patient’s most likely source of methcathinone was
bath salts.
93
An alternative source results from
the metabolism of N,N-dimethylcathinone (Fig. 1C), another cathinone that is known to be abused.
94
We ruled out the latter source (N,N-dimethylcathinone) because
neither the blood sample nor the urine sample contained methylephedrine, the major metabolite of N,N-dimethylcathinone.6
95
It is possible that the laboratory misidentified as
methcathinone another synthetic cathinone that did not undergo phenyl-ring substitution.
96
The addition of alkyl groups at the carbon or nitrogen atoms of the propyl side chain (Fig. 1C) produces
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.
97
Of the 34 designer cathinones listed by Kelly,3 12 are likely to have
ultraviolet spectra that would cause them to be mistaken for methcathinone.
98
Tandem mass spectrometry can differentiate between
methcathinone and methcathinone look-alikes but is not available 24 hours a day.
99
The positive result on the urine test for amphetamines is also directly attributable to the use of
methcathinone.
100
When we assayed standard d,l-methcathinone solutions using
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).
101
This cross-reactivity is understandable given the similarity in
structure of methcathinone and methamphetamine (Fig. 1A), the target analyte in the urine test for amphetamines.
102
The methcathinone metabolite ephedrine probably also contributed to the
observation of immunoreactive amphetamines in the patient’s urine.
103
We concluded that methcathinone is the major finding in the patient’s blood sample that is indicative of the use of
bath salts.
104
We also concluded that methcathinone cross-reacted in this hospital’s KIMS (kinetic interaction of microparticles in solution)
urine immunoassay for amphetamines, contributing to a false positive result.
105
When this patient presented to the emergency department, he showed
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.
106
The diagnosis of cathinone-induced delirium can be a challenge because
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.
107
As in this case, the use of synthetic cathinones often leads to a
false positive screening for amphetamines.
108
Gas or liquid chromatography with mass spectrometry is the standard method for the detection of
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.
109
The clinical presentation of patients with cathinone-induced delirium is similar to the presentation of patients who have taken
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).
110
In this patient, increasingly erratic behavior developed along with
1. paranoia (including delusions of persecution),
2. aggressive and violent psychomotor activity requiring physical restraints,
3. tachycardia, and
4. increased blood pressure.
111
The core triad of symptoms
(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
112
Over the years, the syndrome consisting of these three symptoms has been referred to by many other names
(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
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
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.
114
In patients with cathinone-induced delirium, as in those with malignant catatonia, initial sedation should be achieved with the use of
γ-aminobutyric acid type A (GABAA) agonists such as
1. benzodiazepines or
2. propofol.
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
intravenous haloperidol should be administered judiciously and only after therapy with GABAA agonists is initiated.
116
Monotherapy with dopamine antagonists should be avoided because it may exacerbate the
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.
117
On presentation, this patient was given
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.
118
After the patient’s agitation is under control, attention is turned to minimizing or addressing such medical complications as
1. metabolic acidosis,
2. rhabdomyolysis,
3. hyperthermia, and
4. multisystem failure.
119
This patient received aggressive supportive care, including the administration of
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.
120
Once medical stability has been achieved, then the focus should be on
reversing the neurotransmitter dysregulation induced by synthetic cathinones.
121
One of the challenges in treating cathinone-induced delirium is that there are
multiple synthetic cathinones available and each one has a different receptor profile on the serotonergic, dopaminergic, and noradrenergic systems (Fig. 2).
122
Methcathinone, the substance present in this case, has particularly strong effects on the
dopaminergic and noradrenergic systems, as does methamphetamine;
123
however, methcathinone has a much weaker effect on the serotonergic system than does
methamphetamine.3
124
The treatment strategy after the patient was transferred to the intensive care unit took into account the pathophysiology of
cathinone-induced delirium.
125
The administration of midazolam and propofol was quickly stopped, and
dexmedetomidine, an α2-adrenergic agonist that can ameliorate excess noradrenergic activity, was begun.
126
Low-dose haloperidol administered to the pt as a continuous infusion to treat excess
mesolimbic dopaminergic transmission was also initiated.10
127
To avoid administering a dopamine antagonist alone after dexmedetomidine had been discontinued,
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.
128
The administration of levocarnitine, which facilitates the transport of long-chain free fatty acids across the mitochondrial membrane and thus enhances
antioxidative protection, was also initiated.11
129
On arrival at the intensive care unit, the patient was given
1. propofol and
| 2. midazolam to maintain adequate sedation.
130
On the second day, he was transitioned from propofol and midazolam to
dexmedetomidine and haloperidol administered intravenously by continuous infusion.
131
On the third day, he was extubated but became agitated and had
copious oral secretions that necessitated reintubation and resedation with intravenous propofol and haloperidol by continuous infusion.
132
On the fourth day, the administration of
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.
133
The lactic acidosis resolved by
the second day.
134
Acute renal failure developed owing to a combination of
acute tubular necrosis and rhabdomyolysis;
135
the peak creatine kinase level was
14,965 U (high) per liter, on the third day.
136
The plasma creatinine level peaked at 6.0 mg per deciliter (530 μmol per liter) on the third day, but
the patient maintained sufficient urine output that renal-replacement therapy was not required.
137
The rhabdomyolysis was treated with fluids. Acute liver injury also
developed;
138
aspartate aminotransferase and alanine aminotransferase levels
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.
139
A ventilator-associated pneumonia due to methicillin-sensitive Staphylococcus aureus developed and was treated with
vancomycin and cefepime for 8 days.
140
On the seventh day, hypertension developed and required treatment with
intravenous nitroglycerin.
141
The blood pressure was controlled with
1. oral labetalol,
2. nifedipine, and
3. clonidine.
MLC Unit 3
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