Psychiatric management of Patients in intensive care units.

INTRODUCTION

Since the birth of intensive care medicine in 1953, psychiatrists have played increasingly an important role in providing services to the patients admitted to intensive care unit (ICU). A paper published in JAMA as early as 1965 is one of the first documentations of psychiatric consultation in ICUs.[1]

Significance of the topic is underscored by high prevalence of psychiatric disorders in ICUs, which ranges from below 20% to above 60% according to the type of ICU and assessment methodology[2] and includes various organic brain disorders and other psychopathologies.

SCOPE

The objective of the current guidelines is to provide recommendations to psychiatrists and critical care teams, and the scope includes:

Management of psychiatric problems in ICU patients

Management of psychiatric emergencies arising out of

Suicide attempt

Complications related to alcohol and substance use

Toxicity/complications related to psychotropic medications

Addressing ethical issues, capacity assessment for informed consent for procedures, etc.

Sensitivity to stress and burnout issues in ICU team.

A general approach of psychiatric consultation in ICU is presented first [Figure 1]. Assessment and management of commonly encountered and important conditions for which psychiatric referrals are made in the ICU are elaborated thereafter.

Figure 1

General approach of psychiatric consultation in ICU. ICU – Intensive care unit

CALL TO PSYCHIATRIST FROM THE INTENSIVE CARE UNIT – ACCEPTING CALL TO ATTEND INTENSIVE CARE UNIT PATIENT

By definition, ICU is the place for treatment of the critically ill who deserve to be attended on priority. Paper/electronic medical record notification is often accompanied by verbal/telephonic notification and serves to communicate acceptance of the call to attend the ICU patient. The degree of urgency to attend the call is generally communicated by the referring ICU team, and depending on the setting, the first responder could either be a psychiatry resident or consultant, and reporting/escalation protocol is expected to be in place in case of residents attending the call.

COMMUNICATION WITH REFERRING INTENSIVIST AND GETTING BRIEFING ABOUT THE CASE

Communication with the referring intensivist, either during the referral call or at a subsequent opportunity, provides important opportunity to get briefing about the case including the specific reason for referral. Organic brain disorders top the list of referrals followed by suicide attempts and anxiety/depression [Table 1].[3]

Table 1

Diagnostic break-up of psychiatric referrals in intensive care unit

Diagnosis	Percentage of cases
Mental disorders due to organic causes
Alcohol induced and related disorders	14.56
Acute and chronic organic brain syndrome	19.09
Total	33.65
Suicide attempts	32.69
Anxiety disorders	12.94
Depressive disorders	6.80
Psychotic disorders	3.24
Other psychiatric illness	9.06

*Adapted from Bhogale et al.[3]

GATHERING BACKGROUND INFORMATION

On entering the ICU, it is prudent to obtain all the relevant information about the case available from different sources, viz., medical records – which contain information such as case history and physical examination notes, chart of vitals, reports of laboratory investigations, medical diagnosis, ongoing treatment and interventions, progress notes, and record of behavioral abnormality.

Since patient relatives have limited physical presence in the ICU, nursing staff and resident doctors in the ICU are important source of direct behavioral observation. It is therefore fruitful to spend few minutes interacting with them in addition to reviewing the medical record.

Patient’s caregivers are useful source of prior medical and psychiatric history and treatment, events leading to the ICU admission, and course in the ICU including patient’s behavioral response.

Importance of gathering detailed background information is highlighted by the fact that ICU patients may not be in a condition to provide much details by themselves.

INTERVIEWING INTENSIVE CARE UNIT PATIENT AND CONDUCTING MENTAL STATE EXAMINATION

Interviewing ICU patient/conducting mental state examination (MSE) is a skilled task. Psychiatrist needs to be swift in conducting the mental state and other bedside examination without unduly stressing the patient. Availability of rich background information is therefore very helpful.

Barriers in conducting interview/MSE may include difficulty in comprehension/difficulty in expression or low level of alertness on account of either medical condition or effect of medication. Initial assessment focuses on making quick judgment about the extent to which verbal assessment can proceed, and careful behavioral observation plays very important role in the overall assessment of clinical condition.

ADDITIONAL ASSESSMENT

Physical examination

ICU patient’s general and systemic physical examination including neurological examination findings recorded in case notes is available to a psychiatrist for review who should however conduct any such examination that may be indicated at the time of attending the call.

Additional assessment may include extended neuropsychological assessment or specific scales over and above bedside assessment of MSE. These assessments can be carried out either by the psychiatrist or any other trained personnel.

Additional laboratory tests can be ordered to consolidate the clinical impression and to aid the management and may include biochemical tests (such as drug levels), electrophysiological tests such as electroencephalogram, or brain scan such as magnetic resonance imaging.

DIAGNOSTIC FORMULATION

Diagnostic formulation includes syndromal diagnosis and ascertainment of causality [Figure 2]. Formal classification such as the International Classification of Diseases (ICD) system (current 10th version, and soon to be introduced 11th version) provides clinical descriptions and diagnostic guidelines.

Figure 2

Decision process leading to diagnostic formulation

The psychiatric syndrome/disorder may either be linked to the medical illness or its treatment, or attributable to the stress of illness and environment, or a primary psychiatric disorder including alcohol and substance use.

ICU stay itself could be very stressful. Patients in the ICU experience physical and psychological stress related to the serious and often life-threatening illness, which is compounded by the aspects of ICU environment such as frequent movement of staff, noise of machines, masking of zeitgebers, restrictions on patients regarding mobility and communication, and being witness to adverse outcome of other patients; weakness, fatigue, and cognitive impairment may have additive effect.

MANAGEMENT PLAN AND PRESCRIPTION, WITH DUE CONSIDERATION OF ETHICAL ASPECTS

Very often, quick mitigation of the index behavioral disturbance is expected from the psychiatric referral. However, choice of pharmacotherapy including the agent, dose, and route of administration warrants careful consideration of the following given in Box 1.

Box 1

Considerations in choice of pharmacotherapy

Medical context e.g., compromised hepatic, renal or cardiac status, presence of electrolyte disturbance, history of seizures, etc.

Ongoing medication e.g., anticoagulants, concomitant medications which can interfere with metabolism of psychotropic agents, drug-drug interactions, etc.

Possibility or otherwise of administration through the oral route

Careful dose titration as per medical status of the patient to maximize therapeutic benefit and minimize possibility of adverse effects such as excessive sedation, anticholinergic side effects, and QTc prolongation

In case of ongoing psychotropic medication for preexisting psychiatric condition, decision needs to made either to hold temporarily or stop permanently, to continue or to modify the agent and dose keeping in mind the context and various safety issues mentioned above

A concise note of psychiatric consultation is expected which is able to communicate the inference and management plan with clarity to nonpsychiatrists of ICU team.

Psychological intervention, especially supportive counseling, as permitted by patient’s present state, is helpful in alleviating fear, anxiety, and stress associated with the illness and with ICU milieu.[4]

Briefing ICU staffs about the anticipated response of psychiatric intervention, watching out for any adverse response, and prompt reporting of the same are important steps to ensure quality care. If any PRN prescription is made, it is best to specify the situation which should trigger its use.

Briefing patient relatives about the psychiatric intervention being prescribed is equally important, especially considering the fact that many ICU patients may be in a vulnerable condition unable to consent in true sense. However, due care should be taken to protect confidentiality of patient narrative, particularly when the patient has indicated so, as is often the case in suicide attempt.

Being the place of treatment of critically and terminally ill patients, ICU is also the setting of several ethical dilemmas and considerations, which may range from physical procedures, such as application of restraints, to psychological procedures such as breaking bad news, preparation for end-of-life situation and helping relatives make difficult decisions such as taking patients off life support, and facilitation of advance directives. Family satisfaction is related to clinician communication.[5] It could also be the setting to detect foul play and protect the patient and to encourage altruistic actions such as organ donation. COVID-19 situation has generated debate about the role and limitations of teleconsultation for ICU patients.

It needs to be appreciated that family members may also find the situation challenging and experience depression, anxiety, or anticipatory grief and deserve to be supported as per the need. Prevalence of posttraumatic stress disorder (PTSD) risk is 16%–21% during 6 months postdischarge,[67] and relatives can be made aware about availability of psychiatric help should they need it.

FOLLOW-UP

No quality management plan is complete without follow-up. The frequency of follow-up is often mutually worked out between the intensivist and the psychiatrist and may include postdischarge visits for continuation of psychiatric intervention.

The point prevalence of PTSD symptoms in the ICU patients ranged from 15% to 20% after 3–12 months of discharge as shown by recent meta-analysis of 48 studies,[8] and the psychiatrist should be vigilant for timely management of the same. Cognitive dysfunction, particularly after delirium, is also a common sequel (17%–78%) which may persist for up to several years but tends to improve over time,[9] and it is prudent to screen as a routine on the follow-up visit.

Depending on the nature of the case attended in the ICU (e.g., suicide attempt or alcohol withdrawal) and as per the discretion of the psychiatrist, optional sharing of telecontact may be helpful for prompt cognizance of any problem postdischarge pending the scheduled follow-up.

ASSESSMENT AND MANAGEMENT OF COMMON AND IMPORTANT PSYCHIATRIC CONDITIONS IN INTENSIVE CARE UNIT

Delirium

Delirium is the most common organic/neuropsychiatric disorder caused by transient disruption of brain neuronal activity, which is secondary to systemic disturbances. Delirium risk factors include older age, dementia, mechanical ventilation, metabolic acidosis, emergency surgery or trauma, hypertension, APACHE II score, and coma; multiple organ failure poses moderate risk.

The incidence of delirium in a systematic review of 42 studies on 16,595 patients was found to be 31.8% in critically ill patients and even higher in ICU setting ranging from 60% to 87% in medical ICU and up to 89% in survivors of stupor or coma. The incidence of common surgical condition such as hip fracture is 34%–92%.[10] However, it remains underdiagnosed and under-referred, possibly due to difficulty in recognition by the ICU staff at the extreme of symptom presentation. An Indian study found that the prevalence rate in medical/surgical ICU was 68.2%; however, the referral rate to psychiatric team was 1.7%.[11]

Delirium is associated with increased mortality and morbidity, increased incidence of iatrogenic complications, prolonged hospital stay, poor functional and cognitive recovery, and decreased quality of life in addition to increased cost of care and burden to caregivers. Recognizing its significance, Clinical Practice Guidelines for Management in Elderly was brought out by the Indian Psychiatric Society (IPS) in 2018,[12] which provide details of various aspects of management. A brief overview and update is provided for ready reference and to supplement these guidelines.

Clinical presentation

Delirium presents with acute onset of fluctuating cognitive impairment (disorientation, memory disturbance) and disturbance of consciousness/awareness with a reduced ability to attend and shift attention, which is frequently associated with perceptual abnormalities, sleep–wake rhythm dysregulation, disorganized thought process, emotional dysregulation, and abnormal psychomotor activity. A prodromal phase consisting of restlessness, sleep disturbance, anxiety, and irritability may precede few hours or days. Following delirium phenotypes are recognized:[13]

Subsyndromal type

Hypoactive delirium (extreme-catatonic subtype)

Hyperactive delirium (extreme-excited subtype)

Mixed type

The protracted or persistent type.

Hypoactive type is most common (65%) and often under-recognized.

Assessment and management of delirium

Delirium assessment and management: Five Steps: Figure 3.

Figure 3

Delirium assessment and management: Five steps

Management of known risk factors of the delirium

While old age, medical illness, cognitive impairment, and pre-existing brain disorders are nonmodifiable risk factors, whereas several other risk factors could be modifiable, viz., various medicines, especially opioid and GABA-ergic medicine, medications with anticholinergic effects, prolonged and/or uninterrupted sedation, restricted mobility, acute intoxication and withdrawal states, nutritional deficiencies, metabolic disturbances, water and electrolyte imbalances, endocrinopathies especially hypo or hypercortisolemia, poor oxygenation states (viz., hypoperfusion, hypoxemia, anemia), sleep–wake cycle disruption, and uncontrolled pain [Table 2].

Table 2

Risk factors for delirium

Modifiable factors	Nonmodifiable factors
Sensory impairment	Age >65 years
Immobilization	Cognitive impairment
Medicines, polypharmacy	Multiple comorbidities
Acute neurological diseases such as meningitis, encephalitis, acute stroke, and intracranial hemorrhage	Context of delirium, stroke, other neurological diseases including gait disorders, and history of falls
Acute illnesses such as infection, dehydration, trauma/fracture, and HIV infection	Chronic renal or hepatic diseases
Metabolic derangements
Surgery
Environmental factors
Pain
Emotional distress
Sustained sleep deprivation

*Adapted from Fong et al.[14] HIV – Human immunodeficiency virus

Delirium prevention strategies

Considering the negative consequences of delirium, its prevention is of utmost importance. Delirium is considered as one of the six most common preventable conditions observed among hospitalized elderly patients.[13]

Delirium prevention strategies may be pharmacologic and nonpharmacologic. Nonpharmacologic strategies are considered superior and include:

Providing orientation to time, place, person, and situation

Involving family in patient care.

Sensory aids such as hearing aids and correcting glasses

Cognitive stimulation and memory clues

Mobilizing patient early

Noise and light reduction to aid night-time sleep.

Effectiveness of nonpharmacologic strategies was demonstrated by the Hospital Elder Life Program in which hip fracture repair subjects had significant decrease in onset of delirium (32% in the intervention group compared to 50% in the usual care group). A recent meta-analysis of 14 studies of multicomponent nonpharmacological interventions showed reduced incidence of delirium and prevented falls, that is, how decreased length of hospital stay.

Pharmacologic prevention strategy

Pharmacologic prevention strategy includes:

Minimal use of the pharmacologic agents that may contribute or worsen delirium

Judicious use of sedation

Adequate treatment of pain.

Potentially high deliriogenic or anticholinergic drugs are to be best avoided in the treatment of delirium, which include GABA-ergic agents for sedation and control of agitation with the exception of cases of central nervous system-depressant withdrawal, viz., alcohol, benzodiazepines, and barbiturates, or when more appropriate agents have failed. Use of opioid agents should also be avoided and opioid-sparing strategies such as prescription of parecoxib could help in prevention of postoperative delirium.

A meta-analysis revealed that compared to the conventional GABA-ergic agents such as midazolam or propofol for sedation, use of dexmedetomidine was associated with less delirium. Indian Society of Critical Care Medicine survey however found that nearly, all the respondents use midazolam for sedation (95%) followed by propofol (68%) and dexmedetomidine (60%);[15] more awareness could help improve this trend.

REDUCE trial that evaluated the delirium prevention with haloperidol did not show any benefit.[10] Statin therapy meta-analysis also did not support any beneficial action. Perioperative use of prophylactic antipsychotics was found to be useful in reducing the risk of postoperative delirium. A meta-analysis of 38 studies supported role of dexmedetomidine, antipsychotics, and multicomponent interventions in preventing postoperative delirium.[13] Medications which strengthen circadian rhythm such as suvorexant (potent orexin antagonist) and ramelteon (melatonin agonist) were helpful to lower risk of delirium in the elderly patients;[10] results from large randomized controlled trial on prophylactic melatonin (Pro-MEDIC trial) are awaited. Acetyl cholinesterase inhibitors have protective role in patients with dementia.

Society of Critical Care Medicine has developed a group of interventions called the ABCDEF bundle, which incorporate various prevention strategies listed above. The bundle can help decrease delirium.[14] Its A to F ingredients are:

Assessment, prevention, and management of pain

Spontaneous awakening trial

Spontaneous breathing trial

Choice of sedative agent (proper choice)

Delirium monitoring and management

Early mobilization and physical exercise

Family involvement and empowerment

A recent meta-analysis that included 26,384 patients from 11 studies supported effectiveness of bundle interventions in reducing length of hospital stay, proportion of days with coma, and 28-day mortality, although the prevalence and duration of delirium were not altered significantly.[15]

Surveillance and accurate diagnosis

Surveillance is critical to timely detection of delirium. For this, the standardized surveillance tools such as Confusion Assessment Method (CAM), Intensive Care Delirium Screening Checklist, Stanford Proxy Test for Delirium (S-PTD), and Rapid Assessment Test for Delirium (4AT) and diagnostic tools such as CAM for ICU or Memorial Delirium Assessment Scale are helpful.

A multinational survey from 47 countries revealed that delirium monitoring is carried out in 70% of the ICUs, but only 42% used a validated screening tool.[10] Indian Society of Critical Care Medicine survey reported that only 35% of the intensivists were assessing delirium.[16] These surveys underscore the need for training medical personnel at each levels regarding the prevalence and symptoms of delirium, particularly awareness about its subsyndromal form and use of appropriate screening tools.

4AT and S-PTD are newer tools that have 90% and 79% sensitivity and 84% and 90.8% specificity, respectively. Other useful tools are the Richmond Agitation-Sedation Scale, the Sedation-Agitation Scale, and Neelon and Champagne Confusion Scale for nurses. ICD-10 and DSM-5 are the diagnostic gold standards for delirium.

Important points in clinical workup of delirium include:

History – Present and past medical history, risk and precipitating factors including medication history, drug and alcohol history, sudden onset (within hours or days) with a fluctuating course

Physical examination – Careful note of vitals, oxygen saturation, examination of skin for “tracks” (intravenous drug use), signs of infection, and any source of pain

Neurological examination – Re-emergence of pathologic primitive signs such as glabellar tap reflex, rooting reflex, snout reflex, suck reflex, grasp reflex, palmomental reflex, and Babinski sign

MSE (core domains of delirium)

Psychomotor dysregulation – Agitation (floccillation or carphologia), retardation, or mixed presentation

Cognitive deficits – Clouding of consciousness, inattention, i.e., impaired ability to direct, sustain and shift both visual and auditory attention, disorientation of time, place, and person, and memory impairment

Language impairments (rambling, incoherent, or illogical speech)

Disordered thinking – Delusional thinking, abstract thinking, and comprehension

Executive dysfunction

Altered perceptions (illusions and hallucinations)

Circadian rhythm dysregulation: “Sundowning” sleep–wake cycle disturbances with nocturnal worsening

Emotional dysregulation – Affective lability characterized by anxiety, perplexity, fear, sadness, irritability, apathy, anger, or euphoria

Investigations – Various indicated hematologic, biochemical, electrophysiological, and imaging tests are important to uncover the etiology (For details please refer IPS Practice Guidelines for Delirium).

Management of psychiatric and behavioral manifestations of delirium

Pharmacologic treatment is effective for all types of delirium. Antipsychotics are useful in many ways to control agitation and psychosis, to normalize short-term memory and primitive reflexes, and to protect neurons against hypoxic stress and injury.[13]

A systematic review of 28 studies revealed that clinical improvement is seen in about 75% of patients receiving short-term treatment with low-dose antipsychotics. The treatment response rates observed were consistent across different patient groups and treatment settings, and there were no major differences in the response rates between the clinical subtypes of delirium. No significant difference was observed between efficacy of haloperidol and atypical agents, and the dose of antipsychotics is dependent upon the type of delirium being treated.

In hyperactive delirium, moderate dose of haloperidol is considered to be the treatment of choice subject to the patient’s cardiac condition and absence of significant electrolyte abnormalities.[13] In a study of advanced cancer patients with agitated delirium, addition of lorazepam to haloperidol resulted in a significantly greater reduction in agitation at 8 h.[17] When use of haloperidol is not considered desirable or is contraindicated, atypical antipsychotics should be used. More data exist for risperidone and quetiapine, whereas data are limited for olanzapine, aripiprazole, lurasidone, and paliperidone. Sedative potential and half-life are important considerations in choosing any one of them. Clozapine and ziprasidone are best avoided.

It is safe practice before prescribing antipsychotic agents:[13]

Obtaining 12-lead electrocardiogram and measuring QTc

Checking electrolytes and correction of potassium (K) and magnesium (Mg) if required

Reviewing the list of medication to identify agents with propensity to prolong QTc and avoiding/replacing such medicines or inhibitors of CPY3A4

Discontinuing antipsychotic use if QTc increases to greater than 25% of baseline value or is greater than 500 ms

Evidence about the utility of other pharmacotherapeutic agents in the management of delirium[14]

Acetyl cholinesterase inhibitor (rivastigmine, donepezil) in patients of delirium superimposed on known cognitive deficits or a history of recurrent delirium is not encouraging. One study suggested an increased mortality associated with their use, warranting caution. Physostigmine is used as the first-line treatment for central anticholinergic syndrome and antimuscarinic delirium

Melatonin or melatonin agonist ramelteon is helpful in promoting sleep in all types of delirium

Alpha-2 agonists such as dexmedetomidine and clonidine have a role in protecting against neuronal injury and worsening of delirium associated with acute norepinephrine release secondary to hypoxia or ischemia. Primary sedative agents can be changed from GABA-ergic agents such as propofol or midazolam to dexmedetomidine. Clonidine is also other useful alternative, especially to wean patients off dexmedetomidine

Anticonvulsant and other agents with glutamate antagonism or calcium channel modulation such as valproic acid find utility in the management of agitated delirious patients who are poor responders or cannot tolerate antipsychotic treatment; however, the data are limited. Same is true of carbamazepine and gabapentin. Amantadine and memantine could be useful in cases of traumatic brain injury (TBI) and cerebrovascular accident (CVA).

Pharmacologic treatment of hypoactive delirium involves very-low-dose haloperidol given just before sun down or low dose of risperidone or aripiprazole. In case of marked psychomotor activity retardation or presence of features of catatonia in patients without psychosis, use of psychostimulants such as modafinil, methylphenidate, or dextroamphetamine may be considered. Amantadine, memantine, or bromocriptine may be of help in the management of severe psychomotor retardation in cases of TBI and CVA.

Nonpharmacologic treatment of all types of delirium is similar to the nonpharmacologic strategies of prevention of delirium described previously.

Identification of etiology and treatment of underlying medical condition(s)

Definitive treatment of delirium involves accurate identification of the underlying cause and its timely treatment, which is entrusted to ICU consultee team of intensivist and physician/surgeon. Quick and safe correction of malnutrition, dehydration, and electrolyte abnormalities is part of general management, and so also, minimization of use of medicines may contribute to triggering or worsening delirium, whereas specific management is dependent upon the underlying cause(s). Clinicians find the acronym “I WATCH DEATH” useful as a checklist to investigate the underlying cause[1819] [Table 3].

Table 3

Delirium etiology[19]

Etiology	Clinical conditions
Infection	Systemic infections affecting brain, CNS infections
Withdrawal	Alcohol, sedative medication
Acute metabolic	Acid–base/electrolyte imbalance, kidney or liver failure
Trauma	Head injury, heat stroke, hypothermia, surgery, burns
CNS pathology	Seizures, tumor, hydrocephalus, autoimmune encephalitis, vasculitis, etc.
Hypoxia	Congestive heart failure, respiratory failure, hypotension, anemia, carbon monoxide poisoning
Deficiencies	Deficiency of vitamins
Endocrinopathies	Hypothyroidism, hyperparathyroidism, hypo or hyper cortisolemia, hypo or hperglycemia
Acute vascular	Shock, arrhythmias, cerebrovascular accidents, hypertensive encephalopathy
Toxins/drugs	Alcohol and other substances, pesticides, solvents, excess vitamins
Heavy metals	Lead, manganese, mercury

*Adapted from Joseph Bienvenu et al.[19] CNS – Central nervous system

Additional points about management of delirium linked to alcohol withdrawal, a common condition in clinical practice, find mentioned in a later section

Organic brain syndromes linked specifically to adverse reaction/toxicity of psychotropic medication, viz., neuroleptic malignant syndrome (NMS), serotonergic syndrome (SS), and toxicity of mood stabilizer, specifically lithium overlaps with delirium. Although their occurrence is rare, these are potentially serious conditions and it is important that psychiatrists are aware for prompt recognition and early institution of management.

Neuroleptic malignant syndrome

NMS is a life-threatening condition related to adverse reaction to dopamine antagonists or to rapid withdrawal of dopaminergic medications [Table 4] presenting within hours or days as syndrome of altered mental state, muscle rigidity, fever, and autonomic dysregulation with laboratory evidence of muscle injury (e.g., elevated CPK-10 fold rise).[2021] Risk factors include presence of dehydration, physical exhaustion, exposure to heat, hyponatremia, iron deficiency, malnutrition, alcohol, trauma, thyrotoxicosis, psychoactive substances, and presence of a structural or functional brain disorder. Mortality rate seen is 5%–20% and average period of recovery is 7–11 days. IPS Clinical Practice Guidelines for Management of Schizophrenia also touches upon factors associated with risk of NMS.[22]

Table 4

Medications associated with causation of neuroleptic malignant syndrome

Typical antipsychotics	Atypical antipsychotics	Nonneuroleptics with antidopaminergic activity	Dopaminergics (withdrawal)	Others
Haloperidol	Clozapine	Metoclopromide	Amantadine	Lithium
Fluphenazine	Olanzapine	Tetrabenazine	Toclapone	Phenalzine
Chlorpromazine	Risperidone	Reserpine		Dosulepine
Prochlorpromazine	Quetiapine	Droperidol		Desipramine
Trifluoperazine	Ziprasidone	Promethazine Amoxapine		Trimipramine
Thioridazine	Aripriprazole	Diatrizoate
Thiothixene
Loxaapine
Perphenazine
Bromperidol
Clopenthixol
Promazine

Management of neuroleptic malignant syndrome

Being a rare complication, management insight is based on case series and includes

Stopping all dopamine blockers

Starting dopamine agonist medicines if NMS is caused by stopping it.

Supportive care

Adequate hydration, correction of electrolyte imbalance, external cooling (ice packs in axilla, cooling blankets), gastric lavage of ice water, and use of paracetamol

Lorazepam is useful for agitation and clonidine may be used for autonomic instability (hypertension)

Preventive measures for deep vein thrombosis.

Specific measures

Bromocriptine: starting dose is 2.5 mg 2 or 3 times daily, increased by 2.5 mg every 24 h until a response or until reaching a maximum dose of 45 mg/day. The dose is maintained up to 10 days in case of oral antipsychotics and 2–3 weeks in case of depot preparations

Other drugs such as amantadine hydrochloride, levodopa, apomorphine, and dantrolene can also be tried.

Role of ECT is controversial and recommended where nonpharmacological treatment is required or where drug treatment fails.

Restarting antipsychotics

Since recurrence may happen after restarting high-potency antipsychotic or early after recovery, it is prudent to wait for at least 2 weeks for oral antipsychotics or 6 weeks for depot antipsychotics; low-potency antipsychotics are preferred, starting with low dose and up-titration in slow and careful manner.

Serotonin syndrome

SS (serotonin toxicity) is a life-threatening condition resulting from therapeutic drug use, intentional self-overdosing, or an inadvertent interaction between the drugs. Selective serotonin reuptake inhibitors (SSRIs) are one among the most common in overdose and serotonin toxicity occurs in 15% of SSRI-overdose patients.[232526] Severe serotonin toxicity is a medical emergency usually complicated by rhabdomyolysis, hyperthermia, disseminated intravascular coagulation, and adult respiratory distress syndrome. Onset is generally acute <12–24 h with rapid progression. Resolution can be expected within 24 h if uncomplicated, and mortality is low (<1%) when proper treatment is given. Research groups of Sternbach, Hunter, Radomski and colleagues, and Dounkeley have proposed the diagnostic criteria.

Mild cases present with tachycardia, mild hypertension, mydriasis, diaphoresis, shivering, tremor, myoclonus, and hyperreflexia without fever. Hyperthermia (40.8°C), hyperactive bowel sounds, horizontal ocular clonus, mild agitation, hypervigilance, and pressured speech are seen in moderate cases.

Severe cases include hyperthermia (greater than 41.18°C), dramatic swings in pulse rate and blood pressure (autonomic dysfunction), delirium, and muscle rigidity. Complications such as myoglobinuria, seizures, rhabdomyolysis, metabolic acidosis, renal failure, acute respiratory distress syndrome, and respiratory failure may be seen in some cases and rarely diffuse intravascular clotting, coma, and death.

Table 5 depicts the medication groups and different combinations of drug can cause SS.

Table 5

Medications associated with causation of serotonin syndrome

Drugs	Example
MAOs	Phenelzine, isocarboxazid, tranylcypromine, moclobemide
TCAs	Imipramine, amitryptilline, nortryptilline, clomipramine
SSRIs	Fluoxetine, sertraline, escitalopram, citalopam, paroxetine
SNRIs	Venlafaxine, desvenlafaxine, duloxetine, milnacipran
Other serotonin modulator	Vilazodone
Other antidepressants	Mirtazapine, trazodone
Anti-migrane agents	Triptans
Stimulants	3,4-Methyl-enedioxy-methamphetamine, amphetamine

*Adapted from Jacqueline Volpi-Abadie, et al.[26]. MOAs – Monoamine oxidase inhibitors; TCAs – Tricyclic antidepressants; SSRIs – Selective serotonin reuptake inhibitor; SNRIs – Serotonin Norepinephrine reuptake inhibitor

Management of serotonin syndrome

Treatment is mainly supportive. All serotonergic medication is to be stopped first.

Supportive care

Adequate hydration, correction of electrolyte imbalance, external cooling (ice packs in axilla, cooling blankets), and prescription of benzodiazepine for agitation

In case of severe agitation and hyperthermia, 5HT-antagonist cyproheptadine may be used in an initial dose of 12 mg with the addition of 2 mg every 2 h if symptoms persist

Severe hypertension/tachycardia can be managed with esmolol or nitroprusside

In severe cases, chlorpromazine intramuscular injection in dosage of 50–100 mg is used; physical restraints should be avoided as it may contribute to worsening by enforcing isometric muscle contractions

It is advisable to avoid both bromocriptine and chlorpromazine if diagnosis is uncertain and NMS is a possibility

Sedation/paralysis with a nondepolarizing agent and intubation/ventilation may be warranted in severe cases.

Lithium toxicity

Lithium has a narrow therapeutic index and excessive intake or impaired excretion can result in accumulation and toxicity.[27] It finds mention in the IPS Clinical Practice Guidelines for Management of Bipolar Disorder.[28] Early identification is important since ignoring lithium toxicity can have serious consequences, leading to coma and brain damage or even death. Moderate or severe toxicity warrants ICU management.

Excessive intake could result from accidental or intentional ingestion of excessive amount of lithium tablets or through dose modifications for patients on long-term lithium treatment. Impairment of excretion of lithium can be caused by sodium and volume depletion in conditions such as vomiting, diarrhea, fever, renal insufficiency, strenuous exercise, low intake of water, excessive sweating, diet low in sodium, and congestive cardiac failure. Drugs causing reduction of glomerular filtration rate may also cause chronic toxicity. 95% of lithium excretion takes place through kidneys at clearance rate of 10–40 mL/min. Nephrogenic diabetes insipidus, which can be precipitated by long-term lithium treatment itself, leads to reduced urinary concentrating capacity and may lead to toxicity. Elder patients are vulnerable since lithium clearance may be decreased and half-life prolonged.

Lithium toxicity can happen in the context of:

Acute overdose in a person not on lithium therapy

Acute overdose in ongoing lithium therapy, i.e., acute-on-chronic

Chronic over-medication/drug accumulation, which is associated with the most serious toxicity).

Severity of lithium toxicity

Mild toxicity symptoms are nausea, vomiting, tremor, lethargy, fatigue (serum lithium concentration between 1.5 and 2.5 mEq/L).

Moderate toxicity features are confusion, agitation, delirium, tachycardia, and hypertonia (serum concentration between 2.5 and 3.5 mEq/L)

Severe toxicity is characterized by coma, seizures, hyperthermia, and hypotension (serum concentration >3.5 mEq/L).

Treatment principles

Decontamination – Charcoal should be administered if co-ingestants are unknown. Gastric lavage is useful in cases of regular-release preparations and patients presenting early. In case of sustained-release preparations or massive ingestion of regular-release products, whole-bowel irrigation should be considered

Elimination – Hemodialysis is the most appropriate method of lithium removal, particularly in case of severe lithium toxicity or renal failure

Disposition – All patients with features of toxicity, including those with normal serum lithium levels, should preferably be hospitalized for monitoring. Those with moderate or severe symptoms need to be cared for in the ICU. Six-hourly assessment of serum lithium level is advisable after an acute ingestion and should be continued until descending drift is observed. Observation should continue until thepatient is asymptomatic and serum lithium level falls to below 1.5 mEq/L.

Psychosis in the intensive care unit

Historically, “Intensive Care Unit Psychosis,” “Intensive Care syndrome,” “postcardiotomy delirium after heart surgery,” “cardiac psychosis,” and “ICU Syndrome” were some terms used synonymously with delirium.[20]

Almost any medical condition that affects brain can cause an organic psychosis. Another group of patients in ICU for whom psychiatry referral may be made are cases of pre-existing functional psychosis who have developed some medical complications.[293031]

Some common types of organic psychosis are:

Delirium with psychotic features: Most common organic psychosis, discussed in detail in previous section

Psychosis associated with dementia is also common

Other disorders associated with psychosis include head injury, Parkinson’s disease (PD), human immunodeficiency virus infection, and Huntington’s disease.

Psychosis associated with dementia

Other causes presenting with features of dementia, e.g., immune disorders (lupus) endocrinopathies, viz., hypothyroidism, hypercalcemia, and hypoglycemia, vitamin deficiency (thiamine, niacin), or an untreated infection should be ruled out.[30]

Treatment of psychosis in patients with dementia is challenging. There is a black box warning against antipsychotics due to 1.6–1.7-fold increased risk of mortality. Use of risperidone and olanzapine may be justified in some cases of persistent severe aggression and/or psychosis in cases of Alzheimer’s. Polypharmacy should be avoided to minimize drug–drug interactions in elderly patients, and there should be regular review; effect is modest at best.

Psychosis in Parkinson’s disease

Nonmotor symptoms such as hallucinations and delusions can be present in PD. Patients with PD often have hallucinations in which they have insight.[30] Dopaminergic medicines improve motor symptoms but exacerbate psychosis symptoms. The risk of development of psychosis and other psychiatric symptoms increases by 75% when dementia is associated with PD.

Treatment

Common antipsychotics may improve psychotic symptoms but may worsen motor symptoms, and are not a suitable choice. Pimavanserin, a novel antipsychotic agent with serotonin inverse agonist action and low binding affinity to dopamine receptors, has shown a better safety and efficacy profile in psychosis associated with PD; doses needed to be adjusted as per the comorbidities and renal and hepatic dysfunction. The usual dose is 34 mg PO/day in bid doses.

Malignant catatonia

Malignant catatonia is the severe form of catatonia that may need admission in ICU.[31] The management is similar to that of NMS. Electroconvulsive therapies (ECTs) may have beneficial effect.

Status epilepticus in the intensive care unit

Complex partial seizure status or myoclonic status epilepticus may present like psychiatric syndromes and needs to be differentiated and treated according to seizure type with specific anti-epileptic drugs as per the guidelines.

Patient with suicidal attempt in the intensive care unit

Suicide attempt is a self-injurious behavior with a nonfatal outcome in a person who intended to die. About one-third of ICU admissions are patients attempting suicide. Studies have shown that over 50%–95% of theses have history of psychiatric disorder or prior treatment.[323334] Management of suicide attempt is considered in two parts:

Management of patient with attempted suicide

Considering strategies for prevention of further suicidal attempts.

Psychiatric management of survived patient after attempted suicide

Psychiatrist should establish rapport and therapeutic alliance and should approach the patient in a nonjudgmental manner initially asking open-ended questions. The interview could be semi-structured.

Focus should be on present suicidality, specific psychosocial situation, past and family history of suicide, individual’s strengths and vulnerabilities, and modifiable risk factors

Further, assess past history of psychiatric illness and treatment history, previous suicidal attempts and substance abuse[32]

Conduct thorough psychiatric evaluation to establish psychiatric diagnosis, suicidal ideation, and plan and also assess degree of suicidality to avoid further attempts.

Focus on following specific factors or symptoms that increase risk of suicide:

Anxiety

Hopelessness

Commanding hallucinations

Aggression and impulsivity

Intoxication with alcohol

Previous suicide attempts

Childhood physical/sexual abuse

Domestic partner violence

History of previous treatment/hospitalization

Presence of physical illness

Family history of suicide

Recent or concurrent life stressors

Individual’s current living situation and social support.

Patient’s safety is of utmost importance. Safety measures could be:

Keep the patient in an area that can be easily observed, which is safe but nonrestrictive and having no fixtures which may be used for attempting hanging

Light/electricity fixtures should be concealed one

One-to-one continuous observation; wherever possible 24-h attendance by near relatives and friends to encourage safety and social support

Medication should be in the custody of ICU staff who will administer as per orders

Removal of access to lethal weapons such as guns, sharp objects, dupatta, and sari. Provide hospital clothes

Prepare a safety checklist and share it with staff and accompanying person/observer.

Treatment plan

It should be done in collaboration with consultee, and it is divided into pharmacologic and nonpharmacologic interventions.

Pharmacologic interventions

Antidepressants

TCAs should be avoided in patients with suicidal ideation as overdose can prove lethal

SSRIs and SNRIs if used should honor FDA black box warning and alternatives suggested may be followed, particularly in young adolescent patients with agitated depression since they can increase suicidal ideation and plans temporarily in early phase of treatment

Bupropion and mirtazapine can be the alternatives used for depression, both bipolar and unipolar in this group

One study found paroxetine to be more effective than bupropion.

Anxiolytics

Anxiolytics may be used in the initial phase to take care of anxiety symptoms either alone or along with other psychotropic medication.

Antipsychotics

In patients of schizophrenia with suicidal ideation, atypical antipsychotics such as risperidone, olanzapine, ziprasidone, and clozapine are found to be effective in reducing positive symptoms and also negative symptoms to lesser extent. Mortality rate can be potentially decreased by about 85% using clozapine in suicidal schizophrenic patients. In recent studies, addition of aripiprazole to antidepressants in cases of inadequate response showed reduction in depressive symptoms and suicidal ideation.

Mood stabilizers

Lithium is the only mood stabilizer which in addition to stabilization of mood also reduces suicidal ideation

Anticonvulsant mood stabilizers such as carbamazepine, oxcarbazepine, gabapentin, lamotrigine, levetiracetam, pregabalin, topiramate, valproate, and zonisamide are not as such effective in reducing suicidality in patients with epileptic psychosis

Recently, ketamine infusion 0.5 mg/kg is proved to have rapid antidepressant and antsuicidal effect and can be tried in acute situations

Overall, lithium and clozapine have been shown to be effective in reducing suicidality.

Physical therapy

ECTs are effective in reducing suicidality in acute situations. A full trial can be given.

Psychotherapy

Cognitive behavior therapy

Dialectical behavior therapy

Interpersonal psychotherapy in combination with medical therapies has positive effect on managing suicidality

Documentation of assessment and management plan should be meticulous and carefully done. Management plan should be informed to patient.

Considering strategies for prevention of further suicidal attempts

Psychiatric diagnosis may be revealed for the first time after ICU admission on account of suicidal attempt. Studies found that the rate of death in re-attempters ranges from 2.3% to 4%. Another study found that 37.6% of the participants had died all causes at follow-up, of which 7.2% died by suicide and 53% of these within 5 years of the index suicide attempt. Considering this risk, strategy to prevent further suicidal attempts should be followed as follows.

Assessment

Details of psychiatric and medical illness, past attempt(s), and family history of suicide are important to establish clinical diagnosis.

Assess risk factors as given in Table 6, focus on modifiable factors.

Table 6

Risk factors for suicide

Adolescence and old age

Identity as a bisexual or homosexual

Criminal behavior

Cultural sanction for suicide

Disposition of personal property divorced, separated, or single marital status

Early loss or separation from parents

Family history of suicide

Psychotic symptoms

Chronic painful conditions

Hopelessness

Impulsivity

Increasing agitation

Lethality of previous attempt

Living alone

Mental illness, e.g., depression

Low self-esteem

Male sex

Physical illness or impairment

Previous serious attempts

Protestant or nonreligious status

Recent childbirth

Recent loss

Sexual abuse

Unemployment

Increasing stress

Insomnia

Evaluate patient’s strengths and vulnerabilities as mentioned in Table 7.

Table 7

Protective factors

Coping and problem-solving skills

Self confidence

Possesses healthy and well-developed social skills

Family and social support

Positive integration into society

Maintaining positive values and spirituality

Respects cultural and traditional values

Adequate treatment for mental/physical illnesses

Inquiry into presence or absence of suicidal intent or thoughts, suicidal plans, or behaviors must be made in detail. The severity of intent and potential lethality of the plan is assessed. Various tools are available for this purpose [Table 8]. whether the intent is persistent and active is assessed, suicidal communication is verbalized, and suicidal behavior is obvious with self-injurious behavior or previous attempt.

Table 8

Warning signs

Self-expression about suicidal thought

Expressing ideas for suicide

Hopelessness

Emotional pain or distress

Feelings of loneliness

Helplessness

Believing to be a burden to others

Making arrangements for property management (e.g., making will)

Showing worrisome behaviors

Marked change in behavior, mainly in the presence of other warning signs, including

Withdrawal from social situations and connections

A recent feeling of agitation or irritability

Out-of-character anger or hostility

Sleep changes

Scales for assessing suicidal ideation

Scale for suicide ideation-Beck

Beck hopelessness scale

Columbia suicide severity rating scale

Drug overdose, intoxications, and withdrawal states in intensive care unit

Drug overdose

Drug overdose is ingestion or application of a drug or other substances in quantities greater than recommended or typically practiced, which may result in toxic state or even death. Patients after intentional or accidental overdose are often treated in ICU and psychiatric consultation is sought.[2735363738]

Drug toxicity needs to be considered when a patient acutely develops symptoms such as vomiting, diarrhea, seizures, respiratory distress, symptoms of metabolic acidosis, symptoms suggesting multisystem disorder, shock, or coma. Any change in the behavior, cognition, or autonomic function should suggest either withdrawal or new toxic process due to medications used [Table 9].

Table 9

Drug toxicity of some common medicines

Class	Examples of drugs	Action	Antidote and dose
Sedatives and hypnotics	Benzodiazepines Nonbenzodiazepine GABA agonists Barbiturates ethanol Chloral hydrate	CNS depression	Flumazenil-IV: 0.5 mg over 30 s in adults, to be repeated as per need[36]
Antipsychotics	Typical antipsychotics such as chlorpromazine and haloperidol Atypical antipsychotics such as olanzapine and quetiapine	Hypotension, arrhythmias, and pseudo-Parkinsonian features	Bromocriptine-PO: Start with 1.25-5 mg every 12 h to as high as 10 mg every 6 h Trihexyphenidyl-PO: 2-15 mg/day
Serotonergics	Tricyclic antidepressants, MAO inhibitors buspirone	Tremor Agitation hyperthermia hypertension diaphoresis hyperreflexia clonus, lower extremity muscular hypertonicity diarrhea	Cyproheptadine: 12 mg initial dose followed by 2 mg every 2 h till response
Sympathomimetic psychostimulants	Amphetamines pseudoephedrine phenylephrine ephedrine Cocaine	Hypertension tachycardia agitation paranoia hallucinations Mydriasis piloerection	No specific antidote. Symptomatic with - Sodium bicarbonate, hydralazine, nitroprusside, or phentolamine
Anticholinergics	Atropine, antihistamines Scopolamine Antispasmodic Tricyclic antidepressant Antiparkinsonian agents	Agitation, hallucinations, abnormal movements (e.g., Carphology), tachycardia, mydriasis, dry membranes, hyperthermia, urinary retention, flushed/dry skin	Physostigmine: 0.05 mg/kg IV at a rate not to exceed 0.5 mg/min, with doses no more frequent than hourly[36] Sodium bicarbonate For TCAs IV: 50 mEq per dose to address acidemia and/or ECG signs[36]
Opioid substances	Morphine, codeine Heroin, oxycodone, fentanyl, hydrocodone, propoxyphene	CNS depression respiratory compromise miosis bradycardia hypotension, hypothermia pulmonary edema hyporeflexia seizures	Naloxone: IV: Start 0.05 mg with repeat dosing every 15 s to reversal of respiratory depression and/or unconsciousness; once achieved, repeat the same total dose q1h prn. Higher doses (1-2 mg or more) may be useful in a2-adrenergic agonist toxicity[36]

MOAs – Monoamine oxidase inhibitors; TCAs – Tricyclic antidepressants; CNS – Central nervous system; ECG – Electrocardiogram; GABA – Gamma-aminobutyric acid; PO – Postoperative

The clinician should review history and all previous records, note history of previous toxicity or withdrawals, and perform thorough physical examination. In case of doubt, drug screen should be performed. Strongest predictors requiring ICU treatment include respiratory insufficiency, age >55 years, and a Glasgow coma scale <6. The consultee and the liaison psychiatrist should decide whether the psychotropic medication or other medications should be stopped which are not essential (drug wash-out) except those which can cause withdrawal symptoms and change of previous medicine can be considered, e.g., safer drugs may be considered in place of TCAs or monoamine oxidase inhibitors after patient’s condition has stabilized. Though Selective Serotonin Reuptake Inhibitors (SSRIs) are generally safer, due caution should be observed as they can have antiplatelet activity.

Intoxication

It is acute reversible condition resulting from administration of alcohol or drugs which leads to disturbances at the level of consciousness, cognition, perception, affect, or behavior and altering other psychophysiological functions [Table 10].

Table 10

Alcohol and cannabis intoxication

Disorder	Onset	Clinical features	Differential diagnosis	Management
Alcohol intoxication	From 1 h to 24 h	Smell of alcohol in breath, slurred speech, incoordination, unsteady gait, flushed face, nystagmus, irritability, loquacity, mood changes, later coma, death	Head injury, hypoglycemia, postictal states, hepatic encephalopathy, meningitis, encephalitis, and intoxication with other psychoactive substances	Symptomatic maintain circulation, respiration, blood pressure Provide protective environment, correct hydration, hemodialysis in severe case
Cannabis intoxication/toxicity	Short-term memory, impaired attention, concentration Postural hypotension, delirium, panic attacks, anxiety, myoclonic jerking, and psychosis in more severe cases	Hypoglycemia, electrolyte imbalance, CNS infections, traumatic brain injury and intoxication with other psychoactive substances	Supportive care

CNS – Central nervous system

Withdrawal states

Alcohol withdrawal state Delirium Tremens is the commonest withdrawal state and management details are available in review [Table 11].[38]

Table 11

Alcohol withdrawal - Delirium tremens[38]

Disorder	Onset after cessation	Clinical features	Differential diagnosis	Management
DT	Onset within 48-72 h, peak 4-5 days, may last for weeks	Delirium, autonomic instability, delusions, hallucinations, agitated behavior, coarse tremors, 50% patients having seizures may have DT	Delirium due to other causes	Benzodiazepines: Lorazepam, diazepam, chlordiazepoxide haloperidol
			Dementia	Front loading: With diazepam achieve light sedation with 5 mg IV (repeat after 10 min)
			Psychosis	Then 10 mg IV (repeat after 10 min), then 20 mg IV after 10 min then percentage to 20 mg IV per hour till light sedation or CIWR-Ar score <8 achieved
				Symptom triggered: With diazepam: 10-20 mg IV every 1-4 h, repeat doses till CIWA-Ar score <8
				With lorazepam: 4 mg IV to be repeated every 10 min till either of the aim of front loading is achieved
				If severe delirium still persists even after 16 mg IV then 8 mg IV bolus is to be administered[38]

DT – Delirium tremens; CIWA-Ar – Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised; IV – Intravenous

Anxiety disorders in intensive care unit

Anxiety in ICU patients is generally secondary to:

The ICU setting

The patient’s medical illness

The medications.[394041]

Anxiety can be caused by medical conditions including hypoglycemia, hypoxia, and an evolving myocardial infarction. Patients may develop anxiety on account of the medicines which they are receiving, e.g., medicines such as isoproterenol for cardiac rhythm disturbances and theophylline for concomitant pulmonary disease. Mechanical ventilation causes anxiety in patients who find it difficult to wean from ventilation.[394041]

Anxiety may be a manifestation of sedative, alcohol, opiate, nicotine, or antidepressant withdrawal. Nicotine dependence is perhaps the most common withdrawal syndrome encountered in ICU patients with cardiovascular disorders. Fear of death or fear of disability, misconceptions about the illness and concern about prognosis, misinterpretation of displays and alarms from the monitors in the ICU, and restriction of usual activities may all be linked to causation of anxiety in ICU. Illness and hospitalization may affect patient’s ability to handle ongoing real-life problems and may cause anxiety.

Symptoms of panic disorder and other anxiety disorders overlap with symptoms of cardiorespiratory diseases and patients may have pre-existing anxiety disorder. PTSD is common during or after an ICU admission. Factors contributing to PTSD are

Prior psychopathology

Increased benzodiazepine administration

Post-ICU memories of frightening or psychotic experiences during admission.

Management of anxiety disorders in intensive care unit

Pharmacotherapy

Lorazepam is preferred over other benzodiazepines, and dose is adjusted to the minimum effective dose

As pain and anxiety are associated, effective pain management should be done.

Nonpharmacological therapies

Provide accurate medical information

Have a supportive accompanying family member

Explain the roles and meaning of the monitoring equipment

Provide emotional support and reassurance

Help patient to accept the situation as denial can interfere with treatment.

Use of relaxation technique

Brief psychotherapies

Psychoeducation

Crisis intervention

Supportive psychotherapy

Hypnosis.

Depression in intensive care unit

About 17% of patients admitted in ICU have history of taking SSRIs or SNRIs, and about 28% of ICU survivors report clinically relevant depressive symptoms. Symptoms of depression in ICU may result from:[42]

Acute illness which may directly cause depressive symptoms

Acute illness can produce symptoms that mimic some aspects of depression

Emotional reaction of the patient to acute illness

Secondary to medications

The patient may have an independent major depressive disorder.

Diagnosis

In an ICU setting, it is preferable to err on the side of sensitivity in diagnosing depression as it outweighs the risk of missing potential depression. The Patient Health Questionnaire 2 with cutoff score of 3 in depression has sensitivity of 87.8%, specificity of 71.6. ICD-10/DSM V criteria are the gold standard of diagnosis. IPS guidelines for the management of depression in special situations can be referred to.[42]

Treatment

In most patients, illness is time limited and does not require aggressive pharmacotherapy. In ICUs, antidepressants use is often limited

Patients requiring prolonged stays might develop an adjustment disorder with a depressed mood. It may respond to the initiation efforts for rehabilitation or psychotherapy

Stop offending drugs that may be responsible for major depressive disorder (list provided in IPS Guidelines for Depression and Depression in Elderly People)

In critically ill patients, hold antidepressants, and when they become stable, antidepressants can be restarted

The SSRIs are drug of choice in case of established diagnosis on account of effectiveness, better safety profile, and minimum drug–drug interactions

Care should be taken when patients are receiving other medications such as phenytoin sodium, digoxin, or warfarin (monitor blood levels of these drugs as they have low therapeutic index, when one starts SSRIs)

Sertraline, escitalopram, and citalopram have minimal risk of drug–drug interaction

One needs to be cautious while using venlafaxine and desvenlafaxine as it can cause elevation of blood pressure even at therapeutic dose

Buproprion may lower the seizure threshold and has dopaminergic action, so one should be cautious.

ETHICAL ISSUES

ICU care has been observed as high-tech, aggressive, and often risk-filled medical care and ICU team is often confronted with ethical dilemmas, some of which are by-products of advanced technologies and therapies. Common ethical issues in ICU involve informed consent, application of restraint, decisions regarding life-sustaining treatments such as CPR, withholding or withdrawal of life support, and breaking bad news and organ donation.

Informed consent

one of the most important ethical issues and psychiatrist help may be sought for ascertainment of patient’s capacity to consent. A related issue pertains to ascertainment of fitness for undergoing surgery, either in the context of pre-existing psychiatric disorder or new-onset clouding of consciousness or any other psychopathology, and even emotionally challenging situation like amputation.

Restraints

Restraints, whether physical or chemical, limit both movement and autonomy and advocated only when no better option exists and employed with caution.[4344]

MHCA 17 Section 97.1(a) states that physical restraints should only be used when –

It is the only way available to prevent imminent and immediate harm to the person concerned or to others

It is advised by psychiatrist in charge of person’s treatment

Restraints can be used for minimum duration, under one-to-one supervision of trained staff on the advice of a psychiatrist. It should safe; age and gender appropriate and also suitable to size and physical/medical condition of the patient. One should monitor closely for any deterioration. In ICU setup, mittens, wrist and leg belts, or waist belts can be used to avoid not only removing life support tubes and other aids but also not allowing the patient get out of bed.

End-of-life care

Decisions about treatment at the end of life are often seen difficult/complex and psychiatrist may be called for helping the patient’s family and physician. The psychiatrist should consider relevant medical, ethical, and legal issues, and decisions are best made after careful discussion with patient or surrogate.

Managing anticipatory grief

The psychiatrist can also be called to help in breaking the bad news or to facilitate organ donation – both involving dealing essentially with anticipatory grief.

Stress and burnout in intensive care unit team

The impact that ICU’s unique environment can have on healthcare professionals is receiving increased attention. Exposure to high patient mortality, difficult daily workload, and ethical challenges all contribute to excessive stress and resultant burnout. In 2016, Critical Care Societies Collaborative of USA took cognizance of the ICU professional’s burnout and issued “Call for Action” Statement.[45]

Factors associated with burnout [Figure 4] adapted from Kerlin et al.[45]

Burnout includes symptoms of decreased sense of personal accomplishment, emotional exhaustion, and depersonalization. Two large national surveys (French and USA) revealed high level of burnout in critical care physicians – 46.5% and 44%, respectively, and while several factors are contributory [Figure 4], risk is higher in women physicians. Burnout not only impacts adversely personal health and well-being of ICU professionals but also has major adverse consequence for patient care and therefore needs due attention.

Figure 4

Factors associated with burnout adapted from Kerlin et al.[45]

Burnout mitigation strategies

Critical Care Societies Collaborative suggests that both organizational and individual (ICU professionals) role is important, and the clinicians should have “individual accountability for maintaining their own emotional and physical health and for building resiliency in treatment.” It includes several personal skills such as identification of symptoms, developing healthy strategies of self-care, avoiding unhealthy behaviors. Pilot studies of resilience training in ICU physicians and nurses have generated positive signal, and psychiatrist can make useful contribution to offer such training locally.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest