Critically ill patients can experience severe complications, whether they were admitted with a critical condition or their health worsens during their stay. Significant issues include severe hypoxia, shock, multiorgan failure, and cardiac arrest. For instance, survival chances are generally poor in cases of cardiac arrest, especially in non-critical care areas. Patients with monitored ventricular fibrillation (VF) have a better survival rate compared to those in unmonitored settings, where survival rates drop below 5% for VF and less than 1% for asystole.

The DRS ABCDE approach (Danger, Response, Send for Help, Airway, Breathing, Circulation, Disability, Environment/Exposure) is essential for systematically identifying and managing life-threatening situations. This approach is summarised below.

Medical Emergency Teams (METs): Are rapid-response teams activated to assess and manage acutely unwell patients on hospital wards, aiming to prevent further deterioration before severe complications or cardiac arrest occur. Most hospitals have a MET or a similar system. The principles behind METs include.

Opportunity for Intervention: Clinical and physiological decline often happens gradually.

Warning Indicators: Deterioration usually comes with changes in vital signs, which are straightforward and cost-effective to monitor.

Benefits of Early Action: Early intervention, such as administering oxygen or non-invasive ventilation for respiratory issues or fluid therapy for low blood volume, is often more effective than trying to reverse cardiac arrest after it happens.

Available Expertise: The necessary expertise might not be immediately available.

Activating: Learn to recognise signs of deterioration and understand when to activate the MET.

Activation Criteria: MET activation criteria are generally predefined and relate to measurable declines in the ABCDE categories (see Table 7.1).

Emergency Response: Depending on the patient's location and situation, initiate the emergency response. Most hospital rooms have emergency call buttons.

Criteria for Activating the Medical Emergency Team (MET):

Airway: Patent airway, yes or no?

Breathing: Severe respiratory distress, RR < 8 breaths/min, RR > 27 breaths/min, Oxygen saturation < 90% (new)

Circulation: HR < 40 beats/min, HR > 120 beats/min, Systolic BP < 90 mmHg, Unexplained drop in urine output to < 50 mL over 4 hours

Neurology: Sudden decrease in consciousness level (GCS drop > 2 points), Prolonged or repeated seizures

Other: Any significant concern not covered by the above criteria

Initial Assessment and Management Summary. DRS ABCDE Approach.

Danger: Ensure the safety of both the patient and staff. Check for hazards such as exposed electrical wires, smoke, or discarded needles. Wear gloves to minimize exposure to body fluids.

Response: Assess the patient’s responsiveness by calling their name and checking their reaction to stimuli like shaking a limb or performing a sternal rub.

For Unresponsive or Collapsed Patients, activate the Medical Emergency Team

No Signs of Life?

Begin CPR: 2 breaths, 30 compressions.​ Attach defibrillator pads/monitor if available.

​Attempt defibrillation if appropriate

Provide advanced life support when MET arrives

Evaluate and address life-threatening conditions using the ABCDE approach

Signs of Life?

​Administer oxygen and start monitoring Establish IV access and give fluid bolus if necessary

Call MET if activation criteria are met or if deterioration seems imminent

Handover to MET and provide assistance as needed

Airway: Assess the airway for patency and obstruction, and use appropriate measures to clear it and prevent aspiration. Consider airway adjuncts or intubation by experienced staff if necessary.

Breathing: Evaluate the effectiveness and effort of breathing using pulse oximetry. Provide oxygen and consider assisted ventilation if there is a failure to breathe adequately.

Circulation: Reassess vital signs, check for signs of shock, and monitor tissue perfusion and fluid status. Place ECG and non-invasive BP monitors. Obtain IV access and consider fluids and hemodynamic support. Administer IV fluid rapidly in cases of hypovolemic shock and address abnormal cardiac rhythms as needed.

Disability: Evaluate the level of consciousness using the Glasgow Coma Scale (GCS). A score of 8 or less indicates inadequate airway protection. Address any signs of cerebral hypoxia or hypoperfusion.

Environment, Exposure, and Examination: Normalize body temperature and blood glucose levels. Consider antidotes, electrolyte replacement, and other specific treatments as necessary. Conduct a thorough examination and gather a complete patient history.

A 72-year-old man brought into ED by ambulance from home after his neighbor found him on the floor after doing a welfare check. From the collateral history, the man was found on the floor and may have been there anywhere between 1-18 hours. After the neighbour assisted the man back to the couch, he returned 2 hours later to find him on the floor again. The neighbour described that the patient’s cognition and mobility had rapidly deteriorated over the past 4-6 months. He said his house was full of rubbish and the patient was unable to take care of himself.

After admission to the ED a full A to E was conducted finding no abnormalities.

Initial investigations showed: Nil abnormal findings within the FBC, UECs, and LFT. CXR was clear, CT brain and C-spine showed no acute bleeding or fractures. ECG was showing normal sinus rhythm, nil acute ischaemic changes. BGL and urine dipstick again showed nothing abnormal. Whilst examining the patient it is noticed that he is incontinent of urine 2-3 times, appearing to have lost control of his bladder.

The patient is admitted under general medicine for more thorough investigation and management. When the admitting doctor makes it to ED to see the patient, he forms an initial impression that the patient is delirious. He is talking about cooking in his kitchen, asking how his heart surgery went, and believes he is currently in China waiting to see his doctor. The patient’s vital signs are all within normal limits, a sitting to standing BP is unable to be taken due to the patient’s mental state. Examination of the cardiovascular, respiratory, and urogenital system are all unremarkable. Neuro examination reveals bilateral upper limb rigidity with a mild resting tremor and a dominating downwards gaze, with inability to maintain an upwards gaze for more than 2-3 seconds. After documenting the findings, the patient is moved to the general medical ward where he is then seen by a senior consultant. Within 20-30 minutes of arriving to the ward the patient’s delirium appears to have disappeared. He is now able to hold and maintain attention and answer questions with greater accuracy. The patient is alert to place and can recall the event which brought him into hospital. He explains that he feels increasingly weak and keeps falling over, however, this time he was unable to get back to his feet. He states that he was on the ground for around 12 hours. He describes slumping over his kitchen benchtop and lowering himself down once he realised that the power in his legs had been lost. He reports no preceding chest pain, palpitations, SOB, diaphoresis, calf tenderness or sudden neurological deficits. He has a 20-pack year smoking history, and he stopped smoking 15 years ago. His medical history includes an acute myocardial infarction 15 years ago. He was treated with x2 stents and placed on oral anticoagulation. Aside from this he has been otherwise well.

General Approach to the Falls Patient

One way of doing this is to split up the potential causes into syncope/presyncope vs non syncopal. For a patient presenting within the first category, start by targeting cardiogenic and neurogenic related mechanisms which may have caused the fall. This could be due to a cardiac arrhythmia, heart failure, or valvular disease. Neurogenic could be due to a seizure or from a known epileptic seizure. For non-syncope/pre-syncope falls, consider the patient’s environment (i.e., did they trip or slip on a wet surface) medications (benzodiazepines or anti-hypertensives for example). Was the fall preceded by motor loss, if so, was this a functional long-term decline or sudden loss of motor function. Investigate whether there was a loss of sensation, and if so, was this sudden or chronic. For chronic sensation loss consider diabetic neuropathies, myopathies, and retinopathies (i.e., did the patient fall because of diabetic microvascular damage causing visual loss). For sudden onset, consider a CVA, both ischaemic and hemorrhagic. Assess the patient’s vestibular function, proprioception, and vision.

1. ​Medical Risk Factors
• ​Diabetes: Neuropathy, motor neuropathy, sensory-neural neuropathies
•  Parkinson’s disease
•  Previous stroke
•  Sarcopenia/increased frailty
•  Orthostatic hypotension (>20/10mmHg drop in BP) 
• Sensory disturbance (dizziness/vertigo, poor vision, peripheral neuropathy)
•  Incontinence
•  Depression 
• Alcohol and other substances
2. Age-Related Functional Decline
• Sensory changes: Visual, proprioceptive, vestibular​
• Physical changes: BP regulation, central processing, gait, neuromotor function, postural control
• Cognitive changes: Delirium and dementia cause falls, impaired attention, impaired decision making, impaired fear of falling. Slowing gait when walking and talking (or inability to perform a secondary task whilst walking) predicts future falls
3. Diseases Associated with Functional Decline
• ​Neurological (CVA, PD, cerebellar, neuropathy, dementia, delirium, epilepsy) 
• Cardiovascular (arrhythmia, postural hypotension, anatomical. Vasomotor instability)
• GIT (bleeding, D&V, defecation syncope)
• Metabolic (hypothyroid, hypoglycaemia, hypokalaemia, hyponatraemia)
• Urogenital (micturition syncope, nocturia, incontinence)
• Musculoskeletal (arthritis, myopathy, deconditioning)
• Psychological (anxiety, depression)
4. Medications and Toxins
• ​Antihypertensives Psychotropic medications (anxiolytics, anti-depressants, sedative-hypnotics, mostly benzos and anti-psychotics)
• Levodopa
• Narcotic anaelgesics
• Anticonvulsants
• Alcohol and other ‘recreational drugs’ (acute intoxication or chronic use)
5. Extrinsic risk factors: Environmental stuff

• ​Motor signs and symptoms: Tremor (typically resting), unilateral tremor is the most common presenting symptom and sign. Rigidity (may be cogwheel or lead-pipe). Bradykinesia, prior symptoms may include difficulties writing, doing up buttons, a feeling of stiffness or slowness, voice fluctuations. Postural instability.
• Non-Motor: Sensory, autonomic, neuropsychiatric, sleep disturbances.
• Rigidity: Occurs in 80-90% of patients with Parkinson’s disease. Cog-wheeling (rigidity superimposed on tremor) or lead-pipe rigidity. Unilateral in onset and gradually progresses to involve the other side, although asymmetric throughout the course if idiopathic. Contributes to stiffness and pain.
• Bradykinesia: Present in 80% of patients at onset, eventually 100% will have it – hence most common clinical feature. Major cause of disability. Difficult to describe – ‘’weakness’’, ‘’tiredness’’, ‘’incoordination’’. Typically starts with reduced manual dexterity of fingers in upper limbs and dragging of legs, short step, difficulty standing up from a chair or getting out of a car, turning in bed etc.
• Postural Instability: Impairment of centrally medicated postural reflexes causing imbalance and tendency to fall. Usually a late sign. Early onset of postural instability/falls points towards Parkinson’s plus syndromes like PSP/MSA. Major contributor of disability and the motor features that responds least to therapy. Difficulty in crowds. Propulsion/retropulsion
• Parkinsonian Gait: Difficulty getting up from chair/bed. Initial apraxia/freezing. Stooped posture, reduced arm swing. Short and rapid steps – festination. Difficulty stopping and turning around.

• Parkinsonian Gait​: Difficult getting up from chair/bed. Initial apraxia/freezing. Stooped posture, reduced arm swing. Short and rapid steps – festination. Difficulty stopping and turning around.
• Non-Motor Symptoms:​ Very common, about 97% of patients report NMS. Often affect QOL more than motor symptoms. Disordered sleep complications: Excessive daytime sleepiness, reduced sleep efficiency, reduced slow wave sleep, REM sleep behavioral disorder, restless legs syndrome. Neuropsychiatric, anxiety, apathy, bradyphrenia (slowed thinking), depression, dementia, hallucinations. Autonomic dysfunction, erectile dysfunction, constipation, urinary urgency. Sensory, pain, hyposmia (loss of smell).
• Neuropsychiatric Cognitive Impairment: PD dementia – prevalence 40%. Mean duration approximately 11.5 years. Dementia onset at least 1 year after parkinsonism. Subcortical dementia – manifests with psychomotor retardation, memory difficulty and altered personality. Executive dysfunction (decision making, multitasking). Visual hallucinations, psychosis, and delusions are common. 
• Sleep disorders: Sleep difficulty most common non motor symptom. Most common reported is sleep fragmentation and early morning awakening. Causes, nocturia, difficulty turning over in bed, cramps, vivid dreams, pain, dystonia, and depression. Sleep disorders include, excessive daytime sleepiness, restless leg syndrome, REM sleep behavior disorder.
•  Autonomic Dysfunction: Postural hypotension – can also be due to drugs, increases falls risk. Urinary problems – frequency, nocturia, urgency and urge incontinence – reduced bladder capacity due to involuntary detrusor contraction. Constipation – slow colonic transit, very common and important as it interferes with drug absorption. Sexual dysfunction – decreased interest and low drive due to depression, fatigue, bradykinesia, and rigidity. Excessive sexual drive can be associated with medications.
• Absolute exclusion criteria: Cerebellar abnormalities, Gaze palsy, diagnosis of probable behavioral variant FTD or PPA, lower limb parkinsonism for more than 3 years, treatment with dopamine antagonist, absence of observable response to high-dose levodopa. Unequivocal cortical sensory loss, clear limb ideomotor apraxia, or progressive aphasia. Normal functional neuroimaging of the presynaptic dopaminergic system. Documentation of an alternative condition known to produce parkinsonism.
•  Red flags: Rapid progression of gait impairment (WC bound within 5 years). Absence of progression of motor symptoms for 5 years. Early bulbar dysfunction like dysphonia, dysarthria, or dysphagia within first 5 years. Severe autonomic failure in first 5 years of disease. Recurrent falls in first 3 years of disease. Dystonia of hand and feet in the first 10 years. Absence of the common non-motor features. Pyramidal tract signs. Bilaterally symmetrical parkinsonism.
• Investigations: Cranial imaging, done to exclude specific structural abnormalities (e.g., hydrocephalus, tumor, or lacunar infarcts). DaTscan – Dopamine transporter scan (diagnostic method to look for loss of dopaminergic neurons in the striatum). Parkinsonism vs ET but cannot differentiate PD vs Parkinson’s – plus. MIBG scan – tests cardiac sympathetic denervation. Relatively sensitive and specific in differentiating PD vs Parkinson’s plus.
• Management: Levodopa. Dopamine agonists. MAO-B inhibitors. Anticholinergics. Catechol-O-methyl transferase (COMT inhibitors). Surgical (Deep brain stimulation).
• Investigations: CT/MRI (done to exclude specific structural abnormalities (e.g., hydrocephalus, tumor, or lacunar infarcts. DaTscan – Dopamine transporter scan (diagnostic method to look for loss of dopaminergic neurons in the striatum). Parkinsonism vs ET but cannot differentiate PD vs Parkinson’s – plus. MIBG scan – tests cardiac sympathetic denervation. Relatively sensitive and specific in differentiating PD vs Parkinson’s – plus. 

A 45-year-old man is brought into ED by his wife after experiencing 5 days of nausea and vomiting, fatigue, shortness of breath, excessive urination, and 2 days of confusion. The man is difficult to rouse, and his wife seems concerned. She explains that she thinks he caught the flu a week ago and has been continuously getting worse ever since. As you search for the triage admission form you quickly ask whether she had witnessed him suffering any head trauma, falls in the home, any recent hospital admissions, specific medical history, medications, drug and alcohol use, and allergies.

As you find the form you notice the BSL is 26 mmol/L and ketones are 8 mmol/L. Concurrently, the mans wife states that she hasn’t seen him fall over and that he has barely left bed since becoming unwell. She also mentions that he has diabetes. She can’t remember the type but says it’s not the one fat people get.

Some points to unpack

What is a mole?

The mole (mol) is a unit of measurement that is the amount of a pure substance containing the same number of chemical units (atoms, molecules etc.) as there are atoms in exactly 12 grams of carbon-12 (i.e., 6.022 X 1023). So, the mole is the title used for the amount 6.022 x 1023, much the same way the word "slab" is used to represent 24 cold ones. We use the mol to represent the number of substances in chemistry because the numbers of atoms and molecules in each substance is so large. The value given 6.022 x 1023 is called Avogadro’s number, for the scientist (nerd) that found the number of atoms in 12 grams of carbon 12. Why use 12 grams? This is the theoretical atomic mass of the Carbon-12 isotope (6 protons and 6 neutrons). This means that the atomic mass or atomic weight (12 grams) of carbon is equal to exactly 1 mole of carbon.

The molecular formula for glucose is C6H12O6. This means that there are 6 carbon atoms, 12 hydrogen atoms, and 6 oxygen atoms bonded together to make one molecule of glucose. This means that one molecule of glucose weighs (6 x 12.011 + 12 x 1.008 + 6 x 15.999) = an anatomic weight of 180.16

As one mole = 602200000000000000000000 (6.022 X 10^23) this means that one molecule of glucose is absolutely f***k all. Although, in terms of comparison to carbon, this means that 180 grams of glucose = 1 mole.

What’s a millimole? To make things scalable we use millimoles, with 1000 millimoles making up 1 mole. So, 26mmol/L of glucose in this patient is equal to .026 moles of glucose.

What is a mmol/L? For measuring the level of blood glucose this is often represented as the number mmols contained within 1 litre of blood. There are a huge number of other molecules within blood and measuring blood glucose using this method can be inaccurate. To make things easier, 26 mmol/L means this patient has roughly 26 millimoles of glucose per litre of blood or 468mg per litre (1 mole of glucose = 180 grams) to convert to millimoles (180 grams/1000 = 180 mg) so 1 mmol of glucose = 180 mg (180mg x 26 mmol/L = 468 mg). 1000ml of blood does not weigh 1000 grams though and is usually around 1050 grams. This is slightly more than water because blood contains additional components like cells, proteins, and other dissolved substances that increase its density. The exact weight can vary depending on factors like a person's haematocrit (the proportion of red blood cells) and hydration levels.

What are Ketones? Ketones are organic compounds that are produced when the body breaks down fat for energy, typically when there isn't enough glucose (sugar) available, such as during fasting, prolonged exercise, low-carbohydrate diets, or uncontrolled diabetes. Chemically, ketones contain a carbonyl group (C=O) bonded to two carbon atoms.

The three Main types of Ketones Produced in the Human Body are:

• ​Acetoacetate (AcAc) – the first ketone produced during fat metabolism. 
• Beta-hydroxybutyrate (BHB) – although not technically a ketone (due to its chemical structure), it functions as one in the body and is the most abundant ketone. 
• Acetone – a by-product of acetoacetate breakdown, which is often exhaled through the breath, sometimes giving a fruity odor.

Role of Ketones: When glucose is scarce, the liver produces ketones from fatty acids, which can be used by most tissues in the body, including the brain, as an alternative energy source. In diabetes, high levels of ketones in the blood can lead to ketoacidosis, a dangerous condition, particularly in people with type 1 diabetes, where the blood becomes acidic. People with certain conditions, like type 1 diabetes or type 2 diabetes, have difficulty using glucose without insulin because insulin is essential for allowing glucose to enter cells and be used as energy.

Here's How it Works: (Glucose Entry into Cells) After eating, carbohydrates are broken down into glucose, which enters the bloodstream. Insulin, a hormone produced by the pancreas, acts like a key. It binds to insulin receptors on cells (especially in muscle, fat, and liver cells), triggering a process that opens "glucose transporters" (GLUT4) on the cell membrane. These transporters allow glucose to move from the bloodstream into the cell, where it can be used for energy.

Without Insulin: In the absence of insulin, or if cells become resistant to insulin (as in type 2 diabetes), glucose cannot efficiently enter the cells. This leaves glucose stuck in the bloodstream, leading to high blood sugar levels (hyperglycaemia). Meanwhile, the cells are deprived of energy, even though plenty of glucose is available in the blood.

Consequences of Reduced/Absent Insulin and Insulin Resistance: 

Type 1 Diabetes:​​ In this autoimmune condition, the pancreas does not produce insulin at all because the body's immune system mistakenly attacks insulin-producing beta cells. Without insulin, glucose can't enter the cells, so people with type 1 diabetes require insulin injections to regulate blood sugar.

Type 2 Diabetes: In this case, the body produces insulin, but the cells become insulin-resistant, meaning they don't respond properly to insulin. Over time, the pancreas may also produce less insulin. Without proper insulin function, glucose can't enter the cells as easily, leading to elevated blood sugar levels.

Gestational Diabetes (GDM): This form of diabetes is typically defined as hyperglycaemia that is diagnosed or develops during pregnancy. GDM is often divided into classes, primarily diet-controlled GDM (class A1GDM) or GDM requiring pharmacologic treatment of hyperglycaemia (class A2GDM).

The Role of Placental Hormones in Glucose Metabolism During Pregnancy: In a normal pregnancy, the placenta releases hormones that regulate maternal glucose levels.

Human placental lactogen (hPL) is the primary hormone involved:

• ​Increases insulin resistance
• Stimulates insulin secretion and β-cell proliferation to maintain normal blood glucose levels

• ​Growth hormone
• Corticotrophin-releasing hormone
• Human placental lactogen (hPL)
• Prolactin
• Estrogen
• Progesterone

• ​Pancreatic β-cell dysfunction
• Decreased insulin secretion
• Impaired glucose uptake
• Increased liver glucose production
• Maternal hyperglycaemia

1. One-Step Approach
• ​2-hour, 75-gram Oral Glucose Tolerance Test (OGTT)
• Requires fasting
• Provides immediate diagnosis
2. Two-Step Approach
• ​Initial: 1-hour, 50-gram glucose challenge test (non-fasting)
• Follow-up: 3-hour fasting OGTT for abnormal results

• ​Fasting: ≥95 mg/dL
• 1 hour: ≥180 mg/dL
• 2 hours: ≥155 mg/d 
• 3 hours: ≥140 mg/dL