Delirium and hyponatremia
Management of Hyponatremia -administer what? -how quickly should you aim to correct the sodium level? -consequence of correcting the sodium too quickly? What are some symptoms of this? when do they develop?
-Administer IV fluids. -If SIAD is a consideration, restrict the oral intake of free water to 1 liter daily. -Aim to correct sodium no faster than 8-12mEq/L (8-12 mmol/L) over a 24-hour period. Seizures may be caused by severe hyponatremia. They are not caused by rapid correction, but they are an indication for rapid initial correction of the serum sodium. For example, the sodium may be corrected by 4 meq in the first hour; if the patient is clinically improved, the rate may be slowed to correct by 6 meq in the next 23 hours. Consequence of correcting sodium too quickly Osmotic demyelination is often referred to as "central pontine myelinolysis," because the pons is the most frequent site of myelinolysis. However, lesions also occur in other areas of the brain which is referred to as "extrapontine myelinolysis." Osmotic demyelination is not caused by hyponatremia; it occurs when the hyponatremia is corrected too rapidly. The clinical presentation includes a variety of neuropsychiatric symptoms (confusion, quadriplegia, pseudobulbar palsy, catatonia, "locked-in" syndrome, parkinsonism, mutism, or dystonia), which develop several days after the correction of hyponatremia.
AIDA -A -I -D -A
Acute onset and fluctuating course: -Is there evidence of an acute change in mental status from the patient's baseline? Usually obtained from a family member or nurse Inattention -Did the patient have difficulty focusing attention? For example, are they easily distractible or do they have difficulty keeping track of what is being said? -best test is to ask the patient to repeat the days of the week forward and backward Disorganized thinking -Was the patient's thinking disorganized or incoherent, such as rambling or irrelevant conversations, unclear or illogical flow of ideas, or unpredictable switching from subject to subject? Altered level of consciousness -Alert = normal Vigilant = hyperalert Lethargic = drowsy, easily aroused Stupor = difficult to arouse Coma = unarousable
Risk factors for delirium
Advanced age Dementia Dehydration (which may present as a high BUN:creatinine ratio) Psychiatric disorder Sleep deprivation Immobility Pain Sensory impairment (visual or hearing) Malnutrition History of substance abuse Admission to the ICU
Alcohol withdrawal -symptoms -when can symptoms onset? -Treatment of alcohol withdrawal -treatment of alcohol use disorder
Alcohol withdrawal syndrome is characterized by a hyperadrenergic state with tachycardia, hypertension, diaphoresis, and tremors as well as nausea and headache. Alcoholic hallucinosis is accompanied by hallucinations, usually visual or tactile, within 48 hours after the last drink. Delirium tremens is a severe form of alcohol withdrawal where patients may become confused and disoriented. This usually begins 48-72 hours after the last drink. Treatment: -Give benzodiazepine taper for withdrawal symptoms -Add haloperidol for hallucinations and psychotic symptoms -give multivitamins and folic acid; adminitster thiamine before glucose to prevent wernicke encephaopathy Treatment of alcohol use disorder: -group therapy, disulfiram, naltrexone
More evaluating hyponatremia -what do you assess now? -Hypovolemia causes -Hypervolemia causes -euvolemic causes?
Assess Volume status: Hypovolemia: Hypovolemia is supported by a history of vomiting and diarrhea, diuretic use, bleeding or postural dizziness, and physical exam findings of low jugular venous pressure, orthostatic hypotension and decreased skin turgor. The urine sodium concentration can also help; the urine sodium is reduced to <25meq/L in hypovolemia and is >40meq/L in euvolemic hypotonic hyponatremia. The exception is in situations where there is renal salt-wasting due to diuretics, Addison's disease or cerebral salt-wasting. In these situations, the urine sodium may be elevated, even though the patient is hypovolemic. Hypervolemia: History of hypervolemic states such as CHF, renal failure, or cirrhosis with physical exam findings of anasarca and pulmonary edema may indicate hypervolemia. Euvolemia -SIADH -Primary polydipsia
Workup for delirium
CBC BMP Although a head CT is not routinely necessary in the work-up of delirium, a patient with a history of a recent fall and who is on anticoagulation should get one. EEG would be appropriate if there was a history of seizure or possible post-ictal state, but these are not a routine part of a delirium workup. An ABG would be appropriate if there was a history of respiratory compromise or risk factors for an acid-base disorder. A liver function panel should be considered in patients with a history of liver disease, alcohol abuse, or hepatotoxic medications. While a urinalysis may be helpful in evaluating volume status based on the specific gravity, findings of + leukocyte esterase, + nitrites, pyuria (presence of WBCs), and bacteriuria (presence of bacteria) must be interpreted with caution in an elderly woman with a short term indwelling urinary catheter. Epidemiologic studies have shown significant prevalence of asymptomatic bacteriuria in elderly females living in the community (10.6-16%), as well as patients with short term indwelling urinary catheter use (9-23%). Without urinary symptoms, urinary tract infection is very unlikely to be the cause of this patient's delirium and a urinalysis testing poses a risk of inappropriate diagnosis and treatment for UTI. In a patient in whom substance abuse is suspected, workup should also include a urine toxicology screen for drugs of abuse.
Estimating change in serum sodium -equation -how much sodium is in: 3% saline, NS, 1/2 NS, dextrose in water
Change in serum sodium = ((Infusate Sodium + Infusate Potassium) - Serum Na)/(Total Body Water + 1) The infusate sodium content of intravenous fluids are: 3% normal saline 513 mmol/L 0.9% saline 154 mmol/L 0.45% saline 77 mmol/L Dextrose in water 0
Subdural hematoma -common cause, vessels involved? -commonly seen in who? -symptoms -CT findings -Treatment
Common etiology: -Head trauma leading to rupture of bridging veins leading to accumulaiton of blood between the dura and acracnoid membranes common in: elederly and alcoholics Headache with change in mental status, contralateral hemiparesis, focal neurologic findings CT findings: -reveal a crescent shaped concave hyperdensity acutely (hypodense chronically) Tx: neurosurgical evacuation if symptomatic -may regress spontaneously Because the brain atrophies with age, a larger potential space between the brain and skull develops, allowing a subdural hematoma to develop slowly without the severe symptoms that would occur in a younger brain. Although focal lesions in the brain do not commonly cause delirium without a focal neurologic deficit, elderly patients may occasionally present with delirium and a headache as well as no focal neurologic deficits. A careful neurologic exam is necessary for these patients.
dementia vs delerium vs depression
Dementia is a chronic confusional state that develops slowly, over months to years. Delirium is an acute disturbance in consciousness and perception with an underlying medical etiology. Depression is primarily a mood disorder but can present as confusion in older adults. Delirium affects approximately 30% of hospitalized elderly patients who normally live in the community. This number rises to 65% among hospitalized elderly patients who are admitted from nursing homes. The incidence of delirium in patients admitted to the ICU is even higher.
electrolyte imbalance
Electrolyte imbalance is common in the hospitalized patient and can contribute to delirium. Common imbalances include fluctuations in sodium (hypo- or hypernatremia), glucose (hypo- or hyperglycemia), and calcium (hypercalcemia). Changes in acid-base status such as respiratory acidosis or metabolic acidosis can also cause delirium. Fluid and electrolyte shifts during and after surgery are common and can be exacerbated by the administration of excessive or inadequate intravenous fluids and poor oral intake perioperatively. Loop diuretics (e.g. furosemide) and thiazide diuretics (e.g. HCTZ) can cause both hyponatremia, hypernatremia, and hypokalemia.
Evaluating hyponatremia -first thing you look at? -pseudohyponatremia? (caused by what?) -hypertonic hyponatremia (caused by what?) -Hypotonic hyponatremia (broken down into what three categories)
First evaluate serum osmolality -measured osmolality - BUN/2.8 Rule out pseudohyponatremia: Pseudohyponatremia is an artifact of the assay. If an assay is used that measures sodium indirectly, then elevated levels of serum lipids or proteins may cause the sodium level to be falsely elevated. Hypertonic hyponatremia: In hypertonic hyponatremia, osmotically active solutes like mannitol or glucose draw water out of the cells and into the serum, therefore lowering the sodium concentration of the serum. For every 100mg/dL increase in plasma glucose levels, the serum sodium decreases by 1.6-2.4 mmol/L. Hypotonic hyponatremia: Patients with hypotonic hyponatremia may be hypovolemic, euvolemic, or hypervolemic, and each of these states is a associated with a unique differential diagnosis. There are many causes of hypotonic hyponatremia, although diuretic use (especially thiazides) and the syndrome of inappropriate antidiuresis (SIAD) are very common causes. Knowing the volume status will help narrow down the differential diagnosis.
How to choose the appropriate fluid for hyponatremia correction -severe symptoms -Moderate symptoms
For patients with severe symptoms such as coma or seizures or for those with severe hyponatremia that is known to have developed within 48 hours, rapid correction is warranted. In this setting, 3% saline can be used to raise serum sodium level by 1 to 2 mEq/L (1 to 2 mmol/L) per hour but no more than 8-10 mEq/L (8-10 mmol/L) in the first 24 hours. For those with moderate symptoms (headache, muscle cramps or weakness, impaired memory or difficulty concentrating) and unknown duration of hyponatremia, 0.9% saline can be used. Because the risk of osmotic demyelination is higher with chronic hyponatremia, serum sodium should be raised by 0.5-1 mEq/L (0.5-1 mmol/L) per hour.
Hypoactive vs hyperactive delirium
Hypoactive delirium, where patients tend to sleep more, tends to be overlooked, as opposed to hyperactive delirium, where patients are often disruptive.
Hyponatremia -cut off value? -symptoms Hypokalemia -symptoms -ecg changes Hyperkalemia -symptoms -ecg changes
Hyponatremia is defined as a serum sodium level of <136 mEq/L (<136 mmol/L). Clinical manifestations of hyponatremia are largely neurological, and include disorientation, lethargy, weakness, muscle cramps, headache, nausea, vomiting, restlessness, and depressed reflexes. If the hyponatremia is severe or evolves rapidly (e.g., <48 hours), profound complications such as seizures, coma, permanent brain damage, brain herniation, respiratory arrest, and death can result. Hypokalemia and hyperkalemia do not cause altered mental status directly. However, hypokalemia may cause severe muscle weakness, cramps, tetany, paresthesias, muscle tenderness, cardiac arrhythmias, constipation, ileus and hypo- or hyperreflexia, leading to delirium indirectly if there is cardiac or respiratory failure. Hyperkalemia can cause severe muscle weakness or paralysis and cardiac conduction abnormalities, which can also lead to delirium indirectly in the case of cardiac arrhythmias and/or heart failure. In hyperkalemia, tall, peaked T-waves are the first ECG changes, followed by P-R and QRS prolongation and conduction blocks, loss of P-waves, and cardiac arrest as the hyperkalemia becomes more severe. ECG changes in hypokalemia include flattening of T waves, the appearance of U waves, and in severe cases, ST segment depression and prolongation of the QT interval.
Causes of SIADH -most common -drugs that can cause it Evaluation of SIADH
Most common: -Disorders of the lung (small-cell carcinoma, infections, positive pressure ventilation, and acute respiratory failure) -Disorders of the central nervous system (mass lesions, trauma, inflammatory or demyelinating disorders, stroke, hemorrhage, acute psychosis) Less common: -Uncontrolled pain -Tumors in other locations (mediastinal or extrathoracic) -Severe nausea -HIV infection -Drugs associated with SIAD: (Antidepressants, antipsychotics, NSAIDS) Desmopressin, oxytocin, prostaglandin synthesis inhibitors, nicotine, phenothiazine, tricyclics, serotonin reuptake inhibitors, opiate derivatives, chlorpropamide, clofibrate, carbamazepine, cyclophosphamide, vincristine Evaluation for SIADH -Head and chest CT -TSH -urine sodium > 40 -urine osmolality is >100
consequences of delirium -people who develop delirium in the hospital are how many times increase in their one year mortality? -how often does delirium completely resolve
Patients who develop delirium in the hospital have a two-fold increase in their one-year mortality, independent of their underlying medical problems. They also require longer hospitalizations and are more likely to require institutionalization on discharge. Although delirium usually resolves partially with treatment of the underlying cause, more sensitive testing shows that it resolves completely in only 4% of patients by the time of discharge. In 20% of cases it resolves completely by three to six months. Patients with a hypoactive (decreased level of alertness) delirium are at increased risk for developing pressure ulcers, pulmonary emboli and aspiration pneumonia. Patients with a hyperactive delirium may try to get out of bed unassisted, and barriers such as IV poles and urinary catheters may cause them to fall. This may result in injury, further lengthening their hospitalization and increasing the level of assistance they require on discharge. Multifaceted interventions may reduce number of falls in hospitals. In a cluster randomized trial of over 10,000 patients, a fall prevention tool kit consisting of fall risk assessment, fall prevention plan, bed poster alert, and patient/family education resulted in a fall rate of 1.7% in control group vs 1.3% in intervention group (p=0.02, NNT 250). Patients who are confused may not be able to reliably report their symptoms. Patients who are somnolent with their delirium may not eat properly or take their oral medications. Patients may remember their confusion and be frightened by it, causing symptoms of post-traumatic stress disorder. Family members may also become anxious when they perceive that their relative is "acting crazy."
delirium management
Reorientation: -writing date on message board, large clock, hearing aids, glasses normalize sleep wake cycle -avoid interruptions during the night Treat agitation: -A low dose of a neuroleptic, such as haloperidol 0.5mg is often helpful for agitation, when other measures have been ineffective and the patient is at risk for harming herself or others. However, there may be a small increased risk of stroke when using these agents in older adults. Limit pharm and physical restraints: -Pharmaceutical restraints and sedative-hypnotics such as diazepam or diphenhydramine (Benadryl) can actually increase delirium in older patients. If a sleep agent is needed, trazodone is a safer alternative. It should be noted that benzodiazepines are the first-line treatment for delirium caused by alcohol withdrawal. -remove urinary catheters -Physical restraints should only be used if the patient is agitated enough to be an immediate harm to herself or others, and they should be removed as soon as the danger has passed. Decrease risk of falls
SIADH treatment
Restrict fluid and address the underlying cause -if hyponatremia is severe, or if the pateint is significancly symptomatic, cautiously give hypertonic saline -Demeclocycline, (an ADH receptor antagonist), or vaptans (ADH receptor antagonists) can help normalize serum sodium
Criteria for diagnosing delerium -what criteria the criteria called? -how many must be met to diagnose delirium -how can you remember the criteria?
To diagnose delirium and differentiate it from dementia and depression, use a tool called the CAM (short for Confusion Assessment Method). It was developed for older inpatients and it's simple to use. For diagnosis, the first two items and either the third or fourth item must be present. You can remember the four items of CAM by their first letters (A-I-D-A). Assess item 1 with information from others. Nurses and family members are a good resource for this as they often spend more time at the bedside than we do. Assess items 2, 3, and 4 when taking history.
how do you distinguish the causes of hypotonic euvolemic hyponatremia
Urine osmolality is key in determining the presence of antidiuretic hormone (ADH). When ADH is present, the urine osmolality should be >150 mosm/kg, reflecting ADH's effect of concentrating urine. The presence of a low serum osmolality with a high urine osmolality suggests the inappropriate presence of ADH (because ADH should not be present if serum osmolality is low). -Urine osmolality may be <100 mosmol/kg in primary polydipsia, because ADH secretion is shut down and the kidneys respond by maximally diluting the urine. -Urine osmolality may also be low in malnutrition states or beer potomania, where patients' solute intake and stores are very low, causing decreased solute excretion. -It may also occur when there is a "reset osmostat,"and the serum sodium level at which ADH release occurs is lowered, causing stable mild-moderate hyponatremia.
Wernicke-Korsakoff Syndrome -cause, occurs in who? -korsakoff psychosis symptoms -wernickes syndrome symptoms -prevention?
Wernicke-Korsakoff syndrome occurs in patients who are thiamine deficient. Usually this affects patients who have alcoholism, but patients who are malnourished for other reasons can also develop the syndrome. Korsakoff psychosis is characterized by confabulation (filling in of gaps in memory by unconstrained fabrication), amnesia, and confusion. Wernicke's syndrome is characterized by nystagmus, ophthalmoplegia, anisocoria, ataxia, sluggish papillary reflexes, and potentially coma and death. Thiamine is needed for glucose metabolism; therefore, the effects can be exaggerated by delivering glucose without replacing thiamine first. Therefore, alcoholic patients should be given thiamine (e.g. in a "banana bag") before they are given dextrose IV solutions.
Medication causes of delirium
When a cause of delirium is identified, it is often a medication. There are many medications which may be well tolerated by younger patients, but cause delirium in older patients, especially when they are sick or have underlying cognitive impairment. Medications that act on the central nervous system (either directly or as a side effect) commonly cause delirium in the elderly. These include: -benzodiazepines (e.g. lorazepam) -opioids (e.g. morphine or hydrocodone) -anticholinergics (e.g. diphenhydramine, a.k.a. Benadryl) Antihypertensives which act centrally, such as the alpha-2-agonist clonidine, can cause sedation and delirium. Some antibiotics, especially the fluoroquinolones (e.g. ciprofloxacin), cause delirium.
differential for delirium
electrolyte imbalance medication adverse reaction subdural hematoma alcohol withdrawal heart failure hypothyroidism uncontrolled pain UTI