Depressive and Bipolar Disorders
Mood disorders are the most common reason a person walks onto a behavioural health unit, and they are also the most commonly missed on a medical floor, in an obstetric bay, in a nursing home hallway. Depression is not sadness and mania is not happiness — both are sustained changes in the energy, drive, sleep and thinking of a whole person, and both can kill. This chapter teaches you to recognise the depressive and bipolar disorders by their actual clinical shape, to assess before you intervene, to give the medications by mechanism so that the monitoring makes sense rather than being memorised, and to recognise the four emergencies that live inside mood pharmacology: serotonin syndrome, lithium toxicity, hypertensive crisis on a monoamine oxidase inhibitor, and Stevens-Johnson syndrome on lamotrigine. It also teaches you the sentence to say when a person tells you they want to die, and what to do in the next ten minutes.
By the end of this chapter you can
- Differentiate major depressive disorder, persistent depressive disorder, grief and adjustment disorder using duration, function and the quality of the mood.
- Perform a structured depression assessment using SIGECAPS and the PHQ-9, and describe the mental status exam findings expected in severe depression.
- Distinguish mania from hypomania and classify bipolar I, bipolar II, cyclothymia and mixed features by duration, severity and impairment.
- Explain the mechanism, expected onset, and priority monitoring for SSRIs, SNRIs, bupropion, mirtazapine, tricyclics and MAOIs.
- Recognise and respond to serotonin syndrome, lithium toxicity, tyramine-induced hypertensive crisis and antidepressant discontinuation syndrome.
- Plan nursing care and a therapeutic milieu for a person in acute mania and for a person in severe psychomotor retardation.
- Demonstrate therapeutic versus non-therapeutic responses to hopelessness, guilt and grandiosity, and justify why each response lands the way it does.
- Screen for suicide risk directly, build a safety plan with means restriction, and select the least restrictive intervention that keeps a person safe.
- Escalate deterioration using SBAR and state what may and may not be delegated to assistive personnel on a behavioural unit.
Section 1The Depressive Disorders: What You Are Actually Looking At

Depression is a syndrome of energy and drive, not a mood you can talk someone out of
Major depressive disorder is diagnosed when a person has five or more of nine symptoms present most of the day, nearly every day, for at least two weeks, and at least one of those symptoms is depressed mood or anhedonia — the loss of interest or pleasure in things that previously mattered. The other seven are captured by the mnemonic SIGECAPS: Sleep change, loss of Interest, Guilt or worthlessness, low Energy, poor Concentration, Appetite or weight change, Psychomotor agitation or retardation, and Suicidality. The symptoms must cause distress or impairment and must not be better explained by a substance or another medical condition.
Notice what dominates that list. Only two of the nine items are about feeling. The rest are about how the body runs: sleeping, eating, moving, thinking, wanting. This is why telling a person to cheer up is not merely unhelpful but clinically incoherent — you are asking a person whose sleep architecture, appetite regulation and psychomotor speed have all changed to fix that by choosing differently. Students who understand depression as a whole-body syndrome ask better assessment questions: how many hours are you sleeping, when do you wake, what have you eaten today, how long does it take you to get dressed.
Presentations vary by person and by culture. Older adults frequently present with somatic complaints, memory problems and irritability rather than reported sadness, which is why late-life depression is so often mistaken for early dementia — a distinction Chapter 12 develops in detail. Adolescents commonly present as irritable rather than tearful. Many people from communities where emotional distress is stigmatised will describe fatigue, headache, chest pressure or stomach pain, and will be worked up medically for months. None of these people are exaggerating or somatising deliberately; they are describing depression in the vocabulary available to them.
The differential: grief, adjustment, persistent depression and the medical mimics
Grief and depression overlap and can coexist, but they have different shapes. Grief comes in waves triggered by reminders, and between waves a grieving person can still experience pleasure, humour and connection; self-esteem usually stays intact, and thoughts of death are typically about joining or being with the person who died rather than about being worthless. In major depression the low mood is more constant, self-esteem collapses into worthlessness, and thoughts of death are about deserving to die. A person can be bereaved and depressed at the same time, and the presence of grief never rules out treatment.
Persistent depressive disorder is depression that has been present more days than not for at least two years in adults (one year in children and adolescents), often at a lower intensity but with a longer erosion of function. People with this pattern will often tell you this is just who they are — they have no memory of a well baseline. Adjustment disorder with depressed mood follows an identifiable stressor within three months, and the symptoms do not reach the threshold for major depression. Other specifiers matter clinically: peripartum onset, seasonal pattern, catatonic features, and psychotic features (mood-congruent delusions of guilt, poverty or deserved punishment).
Always rule out the mimics before you settle on a psychiatric explanation. Hypothyroidism, anaemia, vitamin B12 and vitamin D deficiency, obstructive sleep apnoea, Parkinson disease, stroke, pancreatic cancer and untreated pain all produce a picture that looks exactly like depression. So do medications: interferon, isotretinoin, corticosteroids, some beta blockers, hormonal contraceptives in susceptible people, and alcohol, which is a depressant that people frequently use to treat the very symptoms it deepens.
| Feature | Uncomplicated grief | Major depressive disorder | Adjustment disorder |
|---|---|---|---|
| Course | Waves triggered by reminders; eases over months | Persistent most of the day, nearly every day, 2 weeks or more | Begins within 3 months of a stressor; resolves within 6 months of it ending |
| Self-esteem | Preserved | Worthlessness, excessive guilt | Usually preserved |
| Capacity for pleasure | Present between waves | Anhedonia is pervasive | Reduced but present |
| Thoughts of death | Wish to be with the deceased | Belief that others are better off; plan may be present | Uncommon; screen anyway |
| Nursing focus | Presence, normalising, connection to supports | Safety, treatment, function, monitoring | Problem-solving, coping, stressor removal |
Assessment done directly: SIGECAPS, PHQ-9 and the mental status exam
The PHQ-9 is nine items scored 0 to 3, mapping directly onto the diagnostic criteria. Scores of 5, 10, 15 and 20 mark the thresholds for mild, moderate, moderately severe and severe depression. Item 9 asks about thoughts of being better off dead or of self-harm; a positive item 9 requires a direct follow-up interview, not a note in the chart. A tool never replaces the conversation — it structures it, tracks change over time, and gives you a number to hand to the provider.
The mental status exam in severe depression has a recognisable signature. Appearance shows self-care decline: unwashed hair, the same clothes for days, weight loss. Motor activity shows psychomotor retardation — slow initiation, few spontaneous movements, long latency before answering — or agitation, with pacing and hand-wringing. Speech is soft, slow and reduced in amount. Affect is constricted or flat and mood is described as empty rather than sad. Thought content carries themes of worthlessness, guilt, hopelessness and death, and in psychotic depression these become fixed delusions. Cognition shows impaired concentration and slowed processing that can look like dementia. Insight is often intact but colourless: the person knows they are ill and does not believe treatment will help.
Record what you observe, not what you infer. Write “remained in bed for the first four hours of shift, required three prompts to attend breakfast, ate two bites” rather than “unmotivated” or “non-compliant.” The first is data another clinician can act on. The second is a judgement that closes thinking down and, in the record, follows the person from admission to admission.
Depression is a sustained syndrome of altered energy, sleep, appetite, movement and thinking — assess it with a structure such as SIGECAPS or the PHQ-9, rule out medical and medication mimics, and document observed behaviour rather than character judgements.
Section 2The Bipolar Spectrum: Mania, Hypomania and Mixed Features
Mania and hypomania: the criteria that decide everything downstream
A manic episode is a distinct period of abnormally and persistently elevated, expansive or irritable mood together with abnormally increased goal-directed activity or energy, lasting at least one week, present most of the day nearly every day — or any duration if hospitalisation is required. During that period three or more of the following are present, or four if the mood is only irritable: inflated self-esteem or grandiosity, decreased need for sleep, pressured speech, flight of ideas or racing thoughts, distractibility, increased goal-directed or psychomotor activity, and excessive involvement in activities with a high potential for painful consequences. The mnemonic DIGFAST holds them. The episode must cause marked impairment, necessitate hospitalisation, or include psychotic features.
Hypomania uses the same symptom list but requires only four consecutive days, requires an unequivocal change in functioning that is observable by others, and — this is the whole distinction — is not severe enough to cause marked impairment, does not require hospitalisation, and involves no psychotic features. If psychosis is present, or if the person needs to be hospitalised, the episode is mania by definition regardless of how long it lasted.
Two details separate students who understand this from students who have memorised it. First, decreased need for sleep is not insomnia: a person in mania sleeps three hours and feels rested and energetic, while a person with insomnia sleeps three hours and feels wrecked. Reduced sleep is both the most sensitive early warning sign of an emerging episode and one of its most reliable accelerants, which is why sleep is a treatment target and not just an observation. Second, the mood in mania is frequently irritable rather than euphoric, particularly when the person is thwarted; the person who becomes verbally explosive when told they cannot leave is not being difficult, they are demonstrating a cardinal feature of the illness.
Bipolar I, bipolar II, cyclothymia and mixed features
Bipolar I disorder requires only one lifetime manic episode. A depressive episode is common and expected, but is not required for the diagnosis. Bipolar II disorder requires at least one hypomanic episode and at least one major depressive episode, and no manic episode ever. Bipolar II is not a milder illness — people with bipolar II spend more cumulative time depressed and carry a suicide risk at least equal to bipolar I. Cyclothymic disorder involves at least two years of fluctuating hypomanic and depressive symptoms that never meet full episode criteria.
The with mixed features specifier applies when symptoms of the opposite pole are present during an episode — for example, a depressive episode carrying racing thoughts, agitation and reduced need for sleep. Mixed states are the highest-risk configuration in all of mood disorder, because they combine the hopelessness and self-loathing of depression with the energy, impulsivity and disinhibition of mania. A person in a mixed state has both the reason and the means. Treat every mixed presentation as elevated suicide risk until assessed.
Rapid cycling means four or more mood episodes in twelve months and predicts a poorer response to lithium. Peripartum onset deserves separate emphasis: postpartum psychosis typically emerges within the first two weeks after delivery, presents with rapidly fluctuating mood, confusion, delusions and command phenomena, is strongly associated with the bipolar spectrum, and is a psychiatric emergency carrying risk to the parent and the infant. It is not severe baby blues and it does not wait for an outpatient appointment.
| Dimension | Mania | Hypomania |
|---|---|---|
| Minimum duration | 7 days, or any duration if hospitalised | 4 consecutive days |
| Symptom count | 3 (4 if mood is only irritable) | 3 (4 if mood is only irritable) |
| Impairment | Marked; work, relationships or safety collapse | Observable change, but function is preserved |
| Psychosis | May be present | Never — its presence makes the episode mania |
| Hospitalisation | Often required | Not required — if needed, it is mania |
| Diagnosis it supports | Bipolar I | Bipolar II (with a major depressive episode) |
The antidepressant trap and the eight-year diagnostic delay
Most people with bipolar disorder first seek help when depressed, not when elevated — hypomania feels productive and is rarely reported as a problem. The average delay between first mood episode and correct diagnosis is measured in years. The clinical consequence is that people with bipolar depression are frequently started on an antidepressant as monotherapy, which can precipitate a switch into mania or hypomania, induce a mixed state, or accelerate cycling. This is one of the most testable safety points in psychiatric nursing.
Prevent it with history. Before any antidepressant is started, ask the screening questions directly: has there ever been a period of at least several days when you needed much less sleep than usual and still felt energetic; when you talked much faster than usual or people struggled to follow you; when you spent money, made commitments or took risks that were out of character. Ask a family member if you can, because insight into past hypomania is often poor. The Mood Disorder Questionnaire exists for exactly this screen. A family history of bipolar disorder, an early age of onset, psychotic depression, and depression that has failed multiple antidepressants all raise suspicion.
Nursing care in acute mania is a small number of things done consistently. Reduce environmental stimulation: a private or low-traffic room, dimmed lighting, no group activity that will escalate. Provide high-calorie finger foods and fluids the person can carry, because someone who cannot sit still will not sit for a tray. Set limits that are brief, firm, consistent and identical across staff, because it is inconsistent limits that divide a team, not the person. Redirect rather than argue — you cannot win a debate with grandiosity and attempting it becomes the confrontation. Protect the person from the consequences of impaired judgement, including financial decisions, sexual disinhibition and driving. Monitor sleep, hydration, weight and exhaustion; a person in unrelieved mania can become physically depleted to the point of danger.
One lifetime manic episode makes it bipolar I; hypomania is the same symptom list without marked impairment, psychosis or hospitalisation — screen every depressed person for past elevation before an antidepressant is started, because monotherapy can precipitate a switch.
Section 3Pharmacology by Mechanism — and the Four Emergencies
Antidepressants: learn the mechanism and the monitoring writes itself
SSRIs block the serotonin reuptake transporter, raising synaptic serotonin. First-line for depression and for most anxiety disorders. Physical side effects — nausea, headache, jitteriness — appear in days; the mood effect takes two to four weeks and sometimes six. Teach this explicitly, because the person who stops at day five because “it made me feel worse and did nothing” is the most common treatment failure in practice. Sexual dysfunction affects a large minority, persists rather than resolving, and is the leading cause of quiet non-adherence — ask about it plainly. In older adults, watch for hyponatraemia from SIADH. With NSAIDs or anticoagulants, bleeding risk rises. Citalopram carries dose-dependent QT prolongation, capped at 40 mg daily and 20 mg in adults over 60 or with hepatic impairment.
SNRIs (venlafaxine, duloxetine) add noradrenergic reuptake blockade; venlafaxine can raise blood pressure at higher doses, and duloxetine is useful when neuropathic pain coexists. Bupropion works on noradrenaline and dopamine, causes no sexual dysfunction, is activating rather than sedating, and aids smoking cessation — but it lowers the seizure threshold and is contraindicated in seizure disorders, in eating disorders with purging or electrolyte derangement, and in abrupt alcohol or benzodiazepine withdrawal. Mirtazapine blocks presynaptic alpha-2 receptors and is strongly sedating and appetite-stimulating at low doses, which makes it an elegant choice for an older adult with depression, insomnia and weight loss. Trazodone is used at low dose for sleep; teach the person to seek emergency care for a painful erection lasting more than four hours, because priapism is a surgical emergency.
Tricyclics block serotonin and noradrenaline reuptake but also muscarinic, histaminic and alpha-1 receptors, producing dry mouth, constipation, urinary retention, blurred vision, sedation and orthostatic hypotension. Their defining safety problem is lethality in overdose: cardiac sodium-channel blockade widens the QRS and causes dysrhythmia and seizures. Dispense limited quantities to a person at risk and know that serum alkalinisation with sodium bicarbonate is the antidote pathway. MAOIs irreversibly inhibit monoamine oxidase and remain effective for atypical and treatment-resistant depression, at the cost of the strictest diet and interaction rules in psychiatry.
| Class / example | Mechanism | Priority teaching and monitoring |
|---|---|---|
| SSRI — sertraline, fluoxetine, escitalopram | Serotonin reuptake blockade | 2 to 4 weeks to effect; sexual dysfunction; hyponatraemia in older adults; bleeding with NSAIDs; QT with citalopram |
| SNRI — venlafaxine, duloxetine | Serotonin plus noradrenaline reuptake blockade | Monitor blood pressure; severe discontinuation syndrome with venlafaxine; helps neuropathic pain |
| Bupropion | Noradrenaline and dopamine reuptake blockade | Seizure threshold lowered — avoid in purging eating disorders, seizure history, alcohol withdrawal; no sexual dysfunction; activating, dose early |
| Mirtazapine | Alpha-2 antagonism; histamine blockade | Sedation and appetite gain at low dose; give at bedtime; useful for weight loss and insomnia |
| TCA — amitriptyline, nortriptyline | Monoamine reuptake plus muscarinic, histaminic, alpha-1 blockade | Anticholinergic burden; orthostasis; lethal in overdose — limit quantity; ECG in older adults |
| MAOI — phenelzine, tranylcypromine | Irreversible monoamine oxidase inhibition | Tyramine-free diet; 14-day washout (5 weeks after fluoxetine); avoid all sympathomimetics and serotonergics |
Emergency one and two: serotonin syndrome and the tyramine reaction
Serotonin syndrome develops within hours of starting, increasing or combining serotonergic agents. Classic combinations include an SSRI with a triptan, tramadol, linezolid, dextromethorphan, St John’s wort, or an MAOI. The clinical triad is autonomic instability (hyperthermia, tachycardia, hypertension, diaphoresis, diarrhoea), altered mental status (agitation, confusion), and neuromuscular excitability — and it is the neuromuscular findings that clinch it: hyperreflexia, tremor, and clonus, most prominent in the lower limbs. Stop the serotonergic agent, support airway and circulation, cool the person, give benzodiazepines for agitation and rigidity, and anticipate cyproheptadine as a serotonin antagonist. Onset is fast and resolution is fast — this is what distinguishes it from neuroleptic malignant syndrome, which develops over days after an antipsychotic exposure, features lead-pipe rigidity with hyporeflexia and markedly raised creatine kinase, is treated by stopping the antipsychotic and giving dantrolene or bromocriptine rather than cyproheptadine, and resolves over days to weeks.
A person on an MAOI who eats tyramine cannot metabolise it, and the resulting noradrenaline surge produces a hypertensive crisis: sudden severe occipital headache, stiff neck, palpitations, sweating, nausea, photophobia and a dangerously elevated blood pressure. Teach the diet as a list the person can actually carry: aged cheeses, cured or smoked or fermented meats, fermented soy products including soy sauce and miso, tap or draft beer, sauerkraut and kimchi, fava beans, yeast extract spreads, and overripe or spoiled foods. Teach the drug list too — no over-the-counter decongestants, no dextromethorphan, no stimulants, no other serotonergic agents, and a fourteen-day washout in either direction (five weeks after fluoxetine because of its long half-life).
Discontinuation syndrome is the third teaching point and the one most often mistaken for relapse. Abruptly stopping an SSRI or SNRI produces FINISH: Flu-like symptoms, Insomnia, Nausea, Imbalance, Sensory disturbances (the electrical “brain zaps”), and Hyperarousal. Paroxetine and venlafaxine are the worst offenders because of short half-lives; fluoxetine rarely causes it. This is not physical dependence in the addiction sense and saying so matters — but it does mean antidepressants must be tapered, never stopped abruptly, and that a person who runs out of a prescription over a weekend may present to you feeling frightening and unwell.
Emergency three: lithium, the narrow window
Lithium remains the most effective agent for bipolar disorder and the only one with robust evidence for reducing suicide. It also has one of the narrowest therapeutic indices in medicine. Target serum level is 0.8 to 1.2 mEq/L for acute mania and 0.6 to 1.0 mEq/L for maintenance; toxicity begins above 1.5 mEq/L, becomes severe above 2.0, and above roughly 2.5 to 3.5 mEq/L haemodialysis is the definitive treatment. Draw the level as a trough, twelve hours after the last dose — a level drawn at the wrong time is worse than no level, because it will be acted upon.
Baseline workup before starting: renal function (BUN, creatinine, eGFR), thyroid function, electrolytes, pregnancy testing, and an ECG in older adults or those with cardiac disease. Lithium is teratogenic, associated with Ebstein anomaly of the tricuspid valve with first-trimester exposure. Ongoing monitoring: levels every five to seven days until stable, then every three to six months, with renal and thyroid studies every six to twelve months, since lithium causes hypothyroidism and nephrogenic diabetes insipidus over time.
Lithium is a salt handled by the kidney like sodium, so anything that lowers sodium or renal perfusion raises the lithium level. Teach it that way and the person will remember it. Dehydration, vomiting, diarrhoea, fever, heavy exercise, sauna use, a low-sodium diet, NSAIDs, thiazide diuretics, ACE inhibitors and ARBs all push the level up. Consistent daily salt and fluid intake — roughly two to three litres unless restricted — is the core self-management skill. Early toxicity is gastrointestinal and neurological: nausea, vomiting, diarrhoea, coarse hand tremor (a fine tremor may be a benign early effect), drowsiness and muscle weakness. Progression brings ataxia, slurred speech, confusion, hyperreflexia, nystagmus, then seizures, coma and cardiovascular collapse.
| Serum lithium | Expected findings | Nursing action |
|---|---|---|
| 0.6 – 1.2 mEq/L | Therapeutic; fine tremor, mild thirst, polyuria, metallic taste may occur | Continue; reinforce salt and fluid consistency; teach sick-day rules |
| 1.5 – 2.0 mEq/L | Nausea, vomiting, diarrhoea, coarse tremor, drowsiness, muscle weakness | Hold the dose, notify the provider, draw a stat level, assess hydration |
| 2.0 – 2.5 mEq/L | Ataxia, slurred speech, confusion, blurred vision, tinnitus, nystagmus, ECG changes | Hold; urgent provider notification; IV fluids; continuous monitoring; NPO if unsafe swallow |
| Above 2.5 mEq/L | Seizures, coma, dysrhythmia, oliguria, cardiovascular collapse | Medical emergency; airway and circulatory support; prepare for haemodialysis |
Emergency four, plus the anticonvulsants, antipsychotics and the fast options
Valproate is effective in acute mania and mixed states. Monitor liver function and platelets, watch for pancreatitis (severe abdominal pain with vomiting), and know it is among the most teratogenic drugs in routine psychiatric use — neural tube defects and neurodevelopmental harm mean it should not be used in a person who could become pregnant without an explicit discussion and reliable contraception. Hyperammonaemia can cause encephalopathy with a normal transaminase panel. Carbamazepine requires baseline and serial complete blood counts for agranulocytosis and aplastic anaemia, causes hyponatraemia through SIADH, induces its own metabolism and that of many drugs including oral contraceptives, and carries a strong association between the HLA-B*1502 allele and Stevens-Johnson syndrome in people of Han Chinese, Thai and other Southeast Asian ancestry — genotype before starting.
Lamotrigine is the best-tolerated agent for the depressed pole of bipolar disorder, and its one serious hazard defines its dosing: Stevens-Johnson syndrome and toxic epidermal necrolysis. Risk is driven by rapid titration, so lamotrigine is increased over weeks. Teach every person one sentence: any new rash, stop the drug and call immediately — do not wait to see if it spreads, and especially not if it involves mucous membranes, blisters or fever. Valproate roughly doubles lamotrigine levels, so the starting dose is halved when they are combined. If a person misses more than five days, the drug is re-titrated from the beginning rather than resumed at the previous dose.
Second-generation antipsychotics — quetiapine, olanzapine, risperidone, aripiprazole, lurasidone, cariprazine — treat acute mania rapidly and several treat bipolar depression. Their monitoring burden is metabolic: weight, waist circumference, fasting glucose or HbA1c, and lipids at baseline and at intervals, plus screening for extrapyramidal symptoms — acute dystonia within hours to days, akathisia, drug-induced parkinsonism, and the late-onset involuntary orofacial and limb movements of tardive dyskinesia, which is screened for with the AIMS and may be irreversible if the drug is continued (Chapter 8 develops this fully). For severe, treatment-resistant, catatonic or psychotic depression, for acute suicidality, and in pregnancy, electroconvulsive therapy is the fastest effective treatment available. Nursing care: informed consent, NPO after midnight, remove dentures, jewellery and hairpins, void before, hold benzodiazepines and anticonvulsants as ordered because they raise the seizure threshold, and hold lithium because of delirium risk. Afterwards expect post-ictal confusion, headache and myalgia; position side-lying, reorient gently and repeatedly, and monitor for the anterograde and retrograde memory disturbance around the treatment period that must be included in consent. Intranasal esketamine and IV ketamine act within hours and require in-clinic administration with at least two hours of monitoring for dissociation and blood-pressure elevation, and no driving that day.
Match the mechanism to the monitoring: serotonin excess gives clonus and hyperreflexia within hours, lithium is a salt whose level rises whenever sodium or renal perfusion falls, MAOIs plus tyramine give occipital headache and hypertensive crisis, and any new rash on lamotrigine means stop and call now.
Section 4What You Actually Say: Communication, Milieu and Delegation
Therapeutic and non-therapeutic responses, side by side
The most common error with a person who is depressed is reassurance. Reassurance feels kind and functions as dismissal: it tells the person their perception is wrong and that you would rather not hear more. The second most common error is problem-solving too early — offering a solution before the person has finished describing the problem, which ends the disclosure. The third is false cheerfulness, which asks the person to perform wellness for your comfort. The alternative is not a script but a stance: acknowledge, stay, ask, and do not flinch.
With a person in mania, the errors invert. Arguing with grandiosity produces confrontation, laughing along with the joke reinforces escalation, and long explanations lose a distractible listener. What works is short sentences, a calm and low voice, a single message repeated identically, and redirection to a lower-stimulation activity. Set limits on the behaviour without moralising about the person: name the behaviour, name the effect, offer an alternative, state the consequence once.
Study the table below the way you would study a drug card. In examination items and in practice, the correct answer is nearly always the response that stays with the feeling, invites more, and does not defend, argue or reassure.
| The person says | Non-therapeutic — and why | Therapeutic — and why |
|---|---|---|
| “My family would honestly be better off without me.” | “Don’t say that — they love you.” Contradicts the person, ends disclosure, and leaves the risk unassessed. | “That sounds like a heavy thing to be carrying. Are you having thoughts of killing yourself?” Stays with the feeling and screens directly. |
| “Nothing is ever going to get better.” | “Of course it will, you just started the medication.” Argues with hopelessness and asks the person to trust your optimism over their experience. | “Right now it feels like this will not change. Tell me what today has been like.” Validates without agreeing that the future is fixed. |
| “This is all my fault. I ruined everything.” | “You have nothing to feel guilty about.” Denies the feeling; guilt in depression does not respond to correction. | “Guilt like that is one of the ways depression talks. What is it telling you about yourself?” Names the symptom and explores content. |
| “I have solved cardiology. I need a phone right now.” | “That is not true and you know it.” Confrontation with grandiosity reliably escalates. | “I can hear how urgent this feels. Phones are available at 4 o’clock. Walk with me to the quiet room.” Acknowledges, states the limit once, redirects. |
| “You are the only one here who gets it. The others are useless.” | “I know, they can be hard to deal with.” Colludes, divides the team, and abandons the person to a fractured plan. | “I am glad talking helps. Every nurse here is working from the same plan — tell me what was not working with them.” Preserves the team and explores the need. |
| “I do not want to talk.” | “Fine, I’ll come back when you’re ready to cooperate.” Punishes withdrawal, which is a symptom. | “That’s all right. I’m going to sit here with you for a few minutes anyway.” Offers presence without demand — often the highest-value intervention in severe depression. |
The milieu is a treatment, and trauma-informed care is how you run it
The therapeutic milieu is the deliberate use of the environment: predictable structure, a posted schedule, community meetings, safe physical space, graded activity, and staff who behave consistently. For a person with severe depression, structure substitutes for absent internal drive — a schedule requires no decision-making, and decision-making is precisely what is impaired. For a person in mania, structure supplies external limits where internal ones have failed. Environmental safety rounds matter concretely: ligature risk assessment of doors, hooks, cords and curtain rails; searching belongings for sharps, cords, belts and medications; and monitoring what enters the unit with visitors.
Do all of that in a trauma-informed way. A large proportion of people admitted to behavioural health have histories of physical or sexual violence, and the routine procedures of admission — a body search, removal of clothing, being told where to sleep, being watched while bathing — reproduce the shape of those experiences almost exactly. So explain before you act, ask permission before you touch, offer genuine choices where choice exists (which staff member does the search, which order tasks happen in, door open or ajar), narrate what comes next, and never surprise a person from behind. A person who becomes distressed during a search is not being obstructive; they may be telling you something about their history that they cannot say in words.
Say the truth about violence out loud in this environment, because students absorb the opposite from media. Mental illness is not a character flaw and it is not a predictor of dangerousness. People living with serious mental illness are substantially more likely to be the victims of violence than its perpetrators, and are at high risk of exploitation, assault and homicide. When a person on your unit does become aggressive, it is nearly always driven by fear, pain, confusion, a request that went unanswered, or an environment that has become intolerable — and it is nearly always preceded by warning signs you can act on.
Delegation on a behavioural unit
The five rights of delegation apply here with an additional layer: assessment, evaluation, teaching and clinical judgement never transfer. On a behavioural unit, what is delegated is usually observation, and observation is where students most often make a licensure-level error — not by delegating the task, but by delegating the interpretation.
Assistive personnel may perform routine safety checks at the ordered interval once trained on the documentation, may sit continuous one-to-one observation, may take vital signs, assist with hygiene and ambulation, record oral intake and output, weigh, escort within the unit, and report exactly what they saw or heard. Insist on verbatim reporting: “he said he had a way to do it if he got out” is usable, “he seemed off” is not. Assistive personnel may not conduct or interpret a suicide risk screen, change an observation level, evaluate whether a medication is working, teach about a drug or a diagnosis, take a report on a new admission, or make a decision about restraint. Those are registered nurse functions and remain so no matter how experienced the technician is or how busy the shift.
The therapeutic response stays with the feeling, screens directly and never argues with hopelessness or grandiosity; the milieu is a treatment delivered trauma-informed; and observation may be delegated while assessment, evaluation, teaching and risk judgement never are.
Section 5Suicide Risk, Safety and Escalation

Screen directly, in plain words, without euphemism
Asking about suicide does not plant the idea, and in mood disorders the question is never optional — the fear of causing harm by asking is what produces the vague, deniable question that gets a vague, deniable answer. Ask plainly: “Are you having thoughts of killing yourself?” Not “you’re not thinking of doing anything silly, are you?” — which tells the person the correct answer, signals your discomfort, and shuts the door.
If the answer is yes, keep going in the same tone. Ask about a plan: what have you thought about doing. Ask about means: do you have access to that — a firearm, medication, a vehicle, a rope. Ask about timing and intent: have you decided when, how close have you come, what has stopped you so far. Ask about previous attempts, because a prior attempt is the single strongest predictor of a future one. Ask about the protective side too: what keeps you here, who would you call. Structured tools such as the Columbia protocol or the Ask Suicide-Screening Questions organise this and are widely mandated, but they support the interview rather than replacing it.
Language commits you to a stance. Say a person died by suicide or attempted suicide. Never “committed suicide” — the phrase carries the residue of crime and sin, and people who have lost someone hear it. Never call an attempt a gesture, a manipulation, or attention-seeking, and never grade an attempt as failed or successful. Ambivalence is universal: the person in front of you almost always wants the pain to stop rather than wanting to be dead, and it is that ambivalence you are working with.
Safety planning, means restriction and levels of observation
A safety plan is written with the person, in their words, and it is a sequence of things to do: personal warning signs, internal coping strategies that do not require anyone else, people and settings that provide distraction, people to ask for help, professionals and crisis numbers, and steps to make the environment safe. Give the person a copy and put a copy in the chart. It is fundamentally different from a “no-suicide contract,” which asks for a promise, has no evidence of effectiveness, and mainly reassures staff.
Means restriction is the intervention with the strongest evidence and the one most often skipped because it is awkward. Many suicidal crises are short-lived and highly method-specific; putting time and distance between a person and a lethal method saves lives. So ask about firearms explicitly and discuss out-of-home storage with a trusted person or a licensed dealer; dispense limited quantities of medication with a lethal overdose profile such as tricyclics and lithium; involve family in locking or removing medications; and address vehicles, cords, belts and sharps in the home environment as concretely as you would address them on the unit.
On an inpatient unit, safety is graded from routine checks at set intervals, through frequent or line-of-sight observation, to continuous one-to-one observation with an arm’s-length requirement. The governing principle is the least restrictive intervention that provides adequate safety, reassessed continually rather than set once. The corollary is that observation level is a nursing assessment decision within provider orders, and never adjusted by an unlicensed staff member or by the person’s reassurance alone. The statutory frame these decisions sit inside — admission status, decision-specific capacity and the legal limits of confidentiality — is developed in Chapter 3.
De-escalation always comes before restraint
Escalation announces itself. Pacing, clenched fists or jaw, rising volume, shorter sentences, refusal to sit, invading space, fixed staring, sudden silence after agitation. Act at that stage, because once a person is beyond a certain point your options narrow to bad ones. Give space — at least two arm’s lengths, no cornering, keep your own exit clear. Reduce stimulation: fewer people, less noise, lower light, one person speaking. Lower and slow your voice rather than raising it. Use short sentences, name what you observe, ask what would help right now, and offer real choices — a quiet room, a walk, a phone call, food, a PRN medication. Honour whatever you offer, because a broken promise on a behavioural unit is remembered for the entire admission.
Seclusion and restraint are emergency interventions used only when there is an imminent risk of harm to the person or others and less restrictive measures have failed, and they are never used for punishment, staff convenience, or a shortage of staff. There is no such thing as a PRN or standing order for behavioural restraint. A licensed independent practitioner must order it, and a face-to-face evaluation is required within one hour. Orders are time-limited: up to four hours for adults 18 and over, two hours for ages 9 through 17, and one hour for children under 9, renewed only after re-evaluation. The person is monitored continuously, with documented attention to circulation, skin integrity, respiratory status, range of motion, hydration, nutrition and toileting at frequent intervals. Release at the earliest possible moment, and debrief afterwards with the person and with the team — both because restraint is a traumatic event and because the debrief is where you find the missed de-escalation opportunity.
| Red flag | Why it is urgent | SBAR escalation |
|---|---|---|
| New plan, access to means, or a stated intent | Shifts risk from ideation to imminent danger | S: Mr. Alvarez has just disclosed a specific plan. B: Admitted 2 days ago for major depressive disorder, sertraline started day 1, one prior attempt in 2019. A: He describes a plan with access to means and declines to say he is safe. R: I have moved him to continuous observation and removed the item — I need you to evaluate now and review the observation order. |
| Clonus, hyperreflexia, agitation and fever after a serotonergic dose change | Serotonin syndrome; can progress to hyperthermia and rhabdomyolysis within hours | S: Possible serotonin syndrome. B: Escitalopram increased yesterday, tramadol given at 0600. A: Temperature 38.9, heart rate 128, diaphoretic, inducible lower-limb clonus, agitated. R: I have held all serotonergic agents and started cooling — I need urgent evaluation, a benzodiazepine order and transfer to a monitored bed. |
| Coarse tremor, vomiting, ataxia or slurred speech on lithium | Lithium toxicity; a narrow window and a rising level | S: Signs of lithium toxicity. B: Lithium 900 mg twice daily, last level 1.1, started ibuprofen for back pain 3 days ago, gastroenteritis since yesterday. A: Coarse tremor, unsteady gait, slurred speech, poor oral intake. R: Dose held — I need a stat lithium level, electrolytes, creatinine and an order for IV fluids. |
| Any new rash on lamotrigine | Stevens-Johnson syndrome and toxic epidermal necrolysis are life-threatening | S: New rash on lamotrigine. B: Dose increased 6 days ago. A: Macular rash on trunk with two oral lesions and a temperature of 38.2. R: Drug held — I need immediate evaluation and I expect this will be permanently discontinued. |
| Occipital headache, stiff neck and severe hypertension on an MAOI | Tyramine hypertensive crisis; risk of intracranial haemorrhage | S: Possible hypertensive crisis on phenelzine. B: Ate at a restaurant on pass this evening. A: Blood pressure 214/126, severe occipital headache, neck stiffness, palpitations, diaphoresis. R: I need you at the bedside now and an order for rapid blood-pressure management and transfer. |
| Confusion, fluctuating mood and delusions within 2 weeks of childbirth | Postpartum psychosis; risk to parent and infant | S: Suspected postpartum psychosis. B: Delivered 9 days ago, family history of bipolar disorder, has not slept in 3 nights. A: Disorganised speech, belief the baby has been switched, will not be left alone with the infant. R: I have arranged continuous supervision and separated care of the infant — I need emergency psychiatric evaluation and an admission decision now. |
Ask about suicide in plain words, build a written safety plan with means restriction rather than a promise, choose the least restrictive intervention and de-escalate long before restraint — and escalate deterioration in SBAR with the action you have already taken.
The chapter in one breath
Depression is a syndrome of energy, sleep, appetite, movement and thought, not a mood a person chooses; screen it with SIGECAPS or the PHQ-9, exclude thyroid disease, anaemia, B12 deficiency, sleep apnoea, alcohol and drug causes, and document behaviour rather than character. One lifetime manic episode means bipolar I; hypomania is the same symptom list without marked impairment, psychosis or hospitalisation, and mixed features carry the highest suicide risk in all of mood disorder. Screen every depressed person for past elevation before an antidepressant is started, because monotherapy can precipitate a switch. Learn the medications by mechanism and the monitoring follows: SSRIs take two to four weeks and cause sexual dysfunction and hyponatraemia, bupropion lowers the seizure threshold, tricyclics are lethal in overdose, MAOIs need a tyramine-free diet, lithium is a salt whose level rises with dehydration, NSAIDs and thiazides, and any rash on lamotrigine means stop and call. Say the therapeutic sentence — stay with the feeling, ask directly about suicide, never argue with hopelessness or grandiosity. Deliver the milieu trauma-informed, delegate observation but never assessment, de-escalate before you ever consider restraint, and escalate in SBAR with the action you have already taken.
Words worth knowing
| Term | What it means |
|---|---|
| Anhedonia | Loss of interest or pleasure in activities that were previously enjoyable; one of the two gateway symptoms of major depressive disorder. |
| SIGECAPS | Mnemonic for the depression criteria: Sleep, Interest, Guilt, Energy, Concentration, Appetite, Psychomotor change, Suicidality. |
| Psychomotor retardation | Observable slowing of movement, speech and thought, with long latency before responses; a mental status finding, not laziness. |
| Persistent depressive disorder | Depressed mood more days than not for at least 2 years in adults (1 year in youth), often at lower intensity than a major episode. |
| Hypomania | At least 4 days of elevated or irritable mood with increased energy, observable by others, without marked impairment, psychosis or hospitalisation. |
| Mania | At least 7 days (or any duration if hospitalised) of elevated or irritable mood with increased activity plus 3 or more DIGFAST symptoms and marked impairment. |
| Mixed features | Symptoms of the opposite pole during a mood episode; combines despair with energy and impulsivity, and carries the highest suicide risk. |
| Decreased need for sleep | Sleeping far less than usual and feeling rested and energetic — distinct from insomnia, and an early warning sign of an emerging episode. |
| Serotonin syndrome | Rapid-onset autonomic instability, altered mental status and neuromuscular excitability with hyperreflexia and clonus after serotonergic excess. |
| Neuroleptic malignant syndrome | Days-long onset of hyperthermia, lead-pipe rigidity with hyporeflexia, autonomic instability and markedly raised creatine kinase after antipsychotic exposure; stop the drug and treat with dantrolene or bromocriptine — contrast with serotonin syndrome. |
| Discontinuation syndrome | FINISH — flu-like symptoms, insomnia, nausea, imbalance, sensory “zaps” and hyperarousal after abrupt cessation of an SSRI or SNRI. |
| Tyramine reaction | Hypertensive crisis with occipital headache, stiff neck and palpitations when a person taking an MAOI eats aged, cured or fermented foods. |
| Lithium trough level | Serum level drawn 12 hours after the last dose; therapeutic 0.6 to 1.2 mEq/L, toxic above 1.5, dialysis territory above roughly 2.5. |
| Stevens-Johnson syndrome | Severe mucocutaneous drug reaction associated with lamotrigine and carbamazepine; any new rash requires immediate cessation and evaluation. |
| Electroconvulsive therapy | Induced seizure under anaesthesia; fastest treatment for catatonic, psychotic or severely suicidal depression, with transient memory disturbance. |
| Safety plan | A written, person-generated sequence of warning signs, coping strategies, supports and crisis contacts, including steps to restrict access to means. |
| Means restriction | Putting time and distance between a person at risk and a lethal method; the intervention with the strongest evidence for preventing death. |
| Least restrictive intervention | The legal and ethical requirement to use the lowest level of restriction that maintains safety, reassessed continually. |
| Trauma-informed care | Practising on the assumption that a trauma history may be present: explain before acting, ask before touching, offer real choices, avoid surprise. |
| Therapeutic milieu | Deliberate use of structure, predictability, safe physical space and consistent staff behaviour as an active treatment. |