Medicine of the elderly Flashcards
Define multi-organ dysfunction syndrome?
Multi-organ dysfunction syndrome (MODS) is a severe, potentially fatal condition in which two or more organ systems fail concurrently due to dysregulated inflammatory response. It often emerges as a complication of sepsis, trauma, or major surgeries. The pathophysiology of MODS involves complex interactions between the host’s immune system and the precipitating event, leading to systemic inflammation, microcirculatory dysfunction, and eventual organ failure.
What are the risk factors for multiple organ dysfunction syndrome?
Risk Factors:
Advanced Age: Elderly patients are at a higher risk for MODS due to age-related decline in organ function and reserve capacity.
Comorbidities: Underlying diseases such as diabetes mellitus, chronic kidney disease, liver cirrhosis, cardiovascular disease, malignancies and immunodeficiency conditions increase the susceptibility to MODS.
Critical Illness: Patients with sepsis, severe trauma or burns, acute pancreatitis or those undergoing major surgery are predisposed to developing MODS.
Name some underlying causes of multi-organ dysfunction syndrome?
Sepsis: Sepsis is one of the most common precipitating factors for MODS. The systemic inflammatory response triggered by infection can lead to widespread endothelial injury and microvascular thrombi formation resulting in multi-organ failure.
Trauma/Burns: Severe trauma or extensive burns cause massive tissue damage leading to systemic inflammatory response syndrome (SIRS), which may progress to MODS if not managed promptly.
Hypoperfusion/Ischaemia: Conditions causing prolonged hypotension such as shock (cardiogenic, hypovolaemic or septic) can result in inadequate perfusion to vital organs culminating into multi-organ failure.
Immunological Dysfunction: Immunosuppression due to chemotherapy, chronic steroid use or underlying immunodeficiency disorders can predispose to severe infections and subsequent MODS.
What is the pathophysiology of multi-organ dysfunction syndrome?
Initial Insult
The process begins with an initial insult, such as sepsis, trauma, burns or acute pancreatitis, which triggers an exaggerated systemic inflammatory response.
Inflammatory Response
This systemic inflammatory response is characterised by the release of pro-inflammatory mediators like cytokines (TNF-alpha, IL-1), complement components and endotoxins.
Simultaneously there is also activation of coagulation pathways and inhibition of fibrinolysis leading to microvascular thrombosis.
Endothelial Damage and Increased Permeability
The released mediators cause damage to the endothelium, resulting in increased vascular permeability. This leads to interstitial oedema and subsequently impaired tissue perfusion.
Tissue Hypoxia
The impaired tissue perfusion results in tissue hypoxia. This hypoxic environment favours anaerobic metabolism leading to lactic acidosis and further cellular dysfunction.
Organ Dysfunction
This vicious cycle of inflammation, endothelial damage and tissue hypoxia culminates into organ dysfunction. Initially it may manifest as single organ failure but can progress to involve multiple organs if not promptly managed.
Immunoparalysis
In later stages, MODS is characterised by immunoparalysis where there is downregulation of pro-inflammatory responses and upregulation of anti-inflammatory responses. This results in the individual being susceptible to secondary infections which can further complicate the clinical course.
What are the investigations for multi-organ dysfunction syndrome?
Laboratory Investigations
Blood tests: A complete blood count (CBC), coagulation profile, liver function tests (LFTs), renal function tests, electrolytes, and lactate levels are essential. Abnormalities in these parameters can indicate dysfunction in various organs such as the liver, kidney or bone marrow.
Blood cultures: These are necessary to identify potential sepsis, a common precipitant of MODS. Cultures should be taken prior to initiating antibiotic therapy.
Arterial blood gases (ABG): This test assesses respiratory function and acid-base balance. It may reveal hypoxaemia or hypercarbia suggestive of pulmonary dysfunction.
Serum biomarkers: Elevated levels of cytokines such as IL-6 or TNF-alpha suggest systemic inflammation which often accompanies MODS.
Radiological Investigations
Chest radiography: This can help identify pulmonary oedema, pneumonia or acute respiratory distress syndrome (ARDS) contributing to MODS.
Ultrasound scans: These may be useful for visualising organomegaly or fluid collections indicative of organ dysfunction. Specific scans like echocardiography can provide information on cardiac function while abdominal ultrasound can assess hepatic and renal structures.
CT scan: This provides a detailed view of organ structures and can identify pathologies such as abscesses, tumours or infarcts that may precipitate MODS.
Haemodynamic Monitoring
Invasive monitoring techniques such as central venous pressure (CVP) measurement, pulmonary artery catheterisation or transoesophageal echocardiography may be required in certain cases to assess cardiovascular function and guide fluid management.
Tissue Biopsy
If specific organ dysfunction is suspected and non-invasive investigations are inconclusive, tissue biopsy might be performed. Histopathological examination can provide definitive diagnosis in conditions like acute tubular necrosis, interstitial nephritis or liver cirrhosis.
Microbiological Investigations
Sputum culture: In patients with respiratory symptoms, sputum culture can help identify causative pathogens.
Urine culture: This is crucial in detecting urinary tract infections which might contribute to MODS.
Cerebrospinal fluid (CSF) analysis: In cases of neurological dysfunction, CSF analysis can aid in diagnosing infections or inflammatory conditions of the nervous system.
What is the treatment for multi-organ dysfunction syndrome?
Identification and treatment of underlying cause
Conduct detailed investigations to identify the primary disease process or trigger for MODS. This may include blood cultures, imaging studies, or other diagnostic tests as appropriate.
Treat the identified cause promptly. This could involve antibiotics for sepsis, surgical intervention for trauma cases, or immunosuppressive therapy in autoimmune conditions.
Supportive care
Maintain haemodynamic stability using fluid resuscitation and vasopressors as needed.
Ensure adequate oxygenation through supplemental oxygen delivery systems or mechanical ventilation in case of respiratory failure.
Nutritional support is essential. Enteral feeding is preferred if possible; parenteral nutrition should be considered if enteral feeding is contraindicated or insufficient.
Prevention of further organ damage
Closely monitor organ functions using laboratory markers, clinical assessment and imaging techniques where applicable.
Implement strategies to prevent complications such as deep vein thrombosis (DVT), stress ulceration and ventilator-associated pneumonia (VAP).
Frequent reassessment
Regularly reassess the patient’s status and response to interventions. Adjust management plan accordingly based on changes in the patient’s condition.
Involve multidisciplinary team including intensivists, pharmacists, dieticians and physiotherapists for comprehensive management.
What are the four stages of the multi-organ dysfunction syndrome?
- Stage 1 - increased volume requirements, mild respiratory alkalosis, oliguria, hyperglycaemia, increased insulin requirements
- Stage 2 - tachypnoea, hypocapnia, hypoxaemia, moderate liver dysfunction and haematologic abnormalities
- Stage 3 - shock, azotaemia (high nitrogen in the blood), acid-base disturbance, significant coagulation abnormalities
- Stage 4 - vasopressor dependent, oliguria or anuria, development of ischaemic colitis and lactic acidosis
What is the definition of dementia?
According to ICD-10, dementia is a syndrome, usually of chronic or progressive nature, which involves impairment of multiple higher cortical functions, such as memory, thinking, orientation, comprehension and language.
Dementia can be a primary neurodegenerative disorder, or secondary to another condition. Secondary dementias may be reversible, and there is overlap between these and delirium.
A mini-mental state examination (MMSE) score of 24 or less out of 30 suggests dementia with scores of 20-24 mild, 13-20 moderate, and <12 severe.
Name some primary neurodegenerative disorders:
Tauopathies with Beta-Amyloid: Alzheimer’s Disease
Tauopathies without Beta-Amyloid: Fronto-Temporal Dementia, Corticobasal Degeneration, Progressive Supranuclear Palsy
Alpha-synucleinopathy: Lewy Body Dementia, Parkinson’s Disease, Multiple
System’s Atrophy
Polyglutamine disorders: Huntington’s Disease
Vascular dementia: though not a primary neurodegenerative disorder, often grouped together with them as such
Name some secondary neurodegenerative disorders:
Infectious:
Neurosyphilis
Encephalitis/meningitis
AIDS-Dementia Complex
Subacute Sclerosing Panencephalitis
Progressive multifocal leuconephalopathy (JC Polyoma Virus in AIDs)
Trauma:
Chronic sub-dural haematoma
Punch-drunk syndrome (dementia pugilistica)
Normal pressure hydrocephalus: triad of gait disturbance (gait apraxia), dementia, urinary incontinence. There is ventricular enlargement on imaging, and removal of CSF via repeated taps/shunts may help. This condition is believed to be due to impaired absorption of CSF at the level of the arachnoid villi, possibly triggered by a bleed or head injury.
Post-ictal state
Toxic:
Alcohol dementia (due to direct toxic effects of alcohol on the brain)
Solvent, metals inc. lead, carbon monoxide, barbiturates
Autoimmune:
Sarcoidosis
Late stage MS
Vasculitis
Metabolic:
Hepatic/uraemic encephalopathy
B1 deficiency (thiamine) i.e. Wernicke-Korsakoff’s
B12 deficiency (cobalamin)
B9 deficiency (folate)
Pellagra (niacin aka nicotinamide/B3 deficiency - triad of dermatitis dementia, diarrhoea)
Electrolyte derangement (sodium)
Glucose derangement
Neoplastic:
Tumours
Hydrocephalus due to posterior fossa tumours
Paraneoplastic syndromes
Congenital:
Myotonic Dystrophy
Wilson’s disease
Endocrine:
Hypothyroidism
Hypoparathyroidism
Functional: Pseudo-dementia in schizophrenia and depression
What are the signs and symptoms of dementia?
In dementia, there is gradual, progressive, impairment of higher cortical function.
Consciousness is not disturbed in the early stages (in comparison with delirium, which can cause acute cognitive decline in the context of fluctuating or altered consciousness).
Memory Loss: Forgetfulness that disrupts daily life and may involve recently learned information.
Difficulty with Familiar Tasks: Challenges in performing routine tasks, such as cooking or handling finances.
Language Problems: Struggling to find the right words or forgetting the names of familiar objects.
Disorientation: Getting lost in familiar places or losing track of time and dates.
Poor Judgement: Impaired decision-making, leading to risky behaviors or neglect of personal hygiene.
Changes in Mood and Behaviour: Shifts in mood, such as increased irritability, anxiety, or depression.
Withdrawal from Social Activities: A decline in social engagement and interest in hobbies or activities.
Personality Changes: Alterations in personality, including increased apathy or agitation.
Difficulty in Abstract Thinking: Struggling with tasks that require abstract thinking, such as managing finances.
What is the most common cause of dementia?
Alzheimer’s disease - caused by a build up of amyloid protein deposits around brain cells and tau protein tangles within brain cells
What are the four features of dementia remembered by the 4 ‘A’s
Amnesia (recent memories lost first)
Aphasia (word-finding problems, speech muddled and disjointed)
Agnosia (recognition problems)
Apraxia (inability to carry out skilled tasks despite normal motor function)
What is the treatment for mild-moderate Alzheimer’s dementia?
acetylcholinesterase inhibitors rivastigamine, galantamine, and donpezil
contradicted when there is a prolonged QT
These drugs cause cholinergic side effects such as diarrhoea, nausea and vomiting, bradycardia, increased salivary production and urinary incontinence
What is the treatment for severe Alzheimer’s dementia?
NMDA inhibitor - memantine
