Altered Consciousness

Real Cases, Real Thinking, Real Medicine

Amie and Ben discuss a case of 47-year-old male who was found collapsed in the street. 

Can Ben figure out what is going on? 

As you listen, ask yourself: can you figure out the diagnosis? What would you have done in the situation?

Links & Resources

• RCPE Education: rcpe.ac.uk/education

Connect With Us

• Email: amie@homeofmedicine.com
• YouTube: Home of Medicine Channel

Disclaimer: All patient stories discussed in Home of Medicine are informed by real patient interactions. However, all identifying details have been removed or appropriately modified to protect patient confidentiality. 

This podcast is intended for education and professional development and should not replace independent clinical judgement or specialist consultation.

Transcript

Host [Dr. Amie Burbridge]: Hello and welcome to the Home of Medicine Podcast with me, Dr. Amie Burbridge, and my ever-faithful host.

 [Dr. Ben Lovell]: Hi, it's Ben here. My name's Ben Lovell, and I am happy to be back for episode number X.

Host [Dr. Amie Burbridge]: This is a podcast in association with the Royal College of Physicians Edinburgh. I have a very interesting case for you today, Ben, and it is a little bit different. It is a case from when I was a registrar, so it was a while ago, but it really sticks in my head because it is an excellent challenge.

Our patient is a 47-year-old man. You are called to the resuscitation department in the emergency department because the ED team is stuck and needs urgent support from the medical registrar. The history is sparse: this gentleman was found unconscious in the street, slumped over to one side. He was entirely alone and does not appear to have any identifiable information on him—no phone, no wallet, and no driving license. You are effectively managing a "Mr. X" with a severely depressed conscious level. What is your immediate approach?

 [Dr. Ben Lovell]: This is right up my street. I love acute medicine in Resus; that is where the most interesting diagnostic puzzles unfold. As I walk down to the department, my mind is already processing rapid cognitive shortcuts to map out a low GCS:

• Structural Intracranial Axis: Has an acute event occurred inside the brain, such as an intracranial hemorrhage or a massive ischemic stroke?
• Metabolic Axis: Is he experiencing profound neuroglycopenia? We must get an immediate capillary blood glucose to rule out a severe hypoglycemia.
• Toxicological Axis: Has he ingested a toxic substance that is depressing his central nervous system? I need to check his pupils immediately; pinpoint pupils would strongly suggest an opioid toxidrome, while benzos present differently.

A 47-year-old patient is still remarkably young. In this age group, you wouldn't typically expect a profound, hypoactive delirium driven purely by standard bacterial sepsis without an obvious source. My initial priorities are ruling out physical trauma, checking metabolic baselines, and screening for hidden ingestions.

It is highly unusual for an individual to be out without a phone or identification nowadays. However, I won't draw too many immediate conclusions from the lack of ID; I am far more focused on solving the physical puzzle of his unconsciousness.

Objective A-E Assessment and Vital Signs

Host [Dr. Amie Burbridge]: You turn up in Resus and find a full team around the bed. They have stabilized his basic airway and breathing mechanics via standard A-E protocols, but they are entirely unsure what has driven his coma. To help narrow it down, they have already performed an unenhanced CT head, which is completely normal, showing no acute hemorrhage or structural infarction. They are debating an MRI, but that takes considerable time. Where do you begin?

 [Dr. Ben Lovell]: I approach the bedside calmly. I dislike chaotic resuscitations; my goal is to execute a rapid, deliberate A-E assessment, which I can easily achieve within 90 seconds to correct abnormalities as I go:

The 90-Second Emergency Framework:

• Airway: I evaluate patency immediately. As a general rule of thumb, when a patient's GCS drops below 7 or 8, the pharyngeal muscles relax, the tongue falls backward, and upper airway secretions accumulate, creating a high risk of asphyxiation. I will give him a physical shake and shout to check responsiveness and ensure his airway is patent without mechanical adjuncts.
• Breathing: I check his peripheral oxygen saturations, listen for equal bilateral air entry with a stethoscope, and peek at the chest X-ray if one is available.
• Circulation: I evaluate his heart rate, cardiac rhythm, and blood pressure, checking peripheral perfusion, pulses, and fluid status.
• Disability: I calculate his exact formal GCS score (eyes, voice, motor responses) to determine if we need to call an anesthetist to secure the airway. I also integrate the capillary blood glucose level directly into this step.
• Exposure: I pull the sheets down fully to look for external clues: hidden active bleeding, asymmetric lower limb swelling suggesting a deep vein thrombosis, large ulcerating infected wounds, or an incarcerated hernia.

Host [Dr. Amie Burbridge]: Here are his objective A-E findings upon your assessment:

• Airway: Patent, with no pooling of upper airway secretions and no mechanical adjuncts in place.
• Breathing: Oxygen saturations are significantly low at 89% on room air, paired with a remarkably depressed respiratory rate of 10 breaths/min.
• Circulation: Heart rate is elevated at 128 bpm in a regular sinus rhythm, paired with a hypertensive blood pressure of 165/95 mmHg.
• Temperature: Febrile at 38.2°C.
• Disability (Glucose): Capillary blood glucose is high at 18 mmol/L.
• Pupils: Bilaterally dilated.

Regarding his GCS, I must admit that I sometimes struggle to recall the exact parameter scoring on the spot. He does not open his eyes spontaneously, he produces non-specific groaning sounds without recognizable words, and he exhibits spontaneous, semi-purposeful thrashing movements of his limbs but does not follow commands. This tracks as a GCS of approximately 13.

 [Dr. Ben Lovell]: An oxygen saturation of 89% is far too low, especially paired with a bradypnea of 10. My immediate action is to apply high-flow oxygen via a 15-liter non-rebreathe mask. While we always keep hypercapnic respiratory drive in mind for chronic conditions, an acutely hypoxic, critically unwell patient requires immediate oxygenation. I will arrange an urgent arterial blood gas (ABG) to check for severe hypercapnia or respiratory failure.

His blood pressure of 165/95 mmHg is elevated, but it is reassuring from a perfusion standpoint; we know his brain and vital organs are receiving adequate blood flow. If his blood pressure were profoundly low, it would easily explain his low conscious level.

A glucose of 18 mmol/L is distinctly abnormal and suggests diabetes, but it isn't low enough to cause neuroglycopenic coma. His dilated pupils are a vital clue: they immediately eliminate simple opioid toxicity from my list, as that would present with classic pinpoint pupils. What does the general exposure reveal?

Host [Dr. Amie Burbridge]: On exposure, he is profoundly diaphoretic and unkempt, with a distinct malodorous scent. His clothes are heavily soiled, which led us to consider if he might be an individual of no fixed abode or experiencing homelessness.

There are no active skin ulcers or signs of intravenous drug injection marks. His calves are soft and non-tender, his heart sounds are normal, and his lungs are clear on auscultation. There are non-specific, minor random ecchymoses across his limbs and chest, but no major trauma. His fingernails and toenails are heavily packed with dirt, confirming a chronic lack of self-care.

Interpreting Metabolic and Infectious Markers

 [Dr. Ben Lovell]: The combination of hypoxia and central hypoventilation means he is likely retaining carbon dioxide, which can directly cause a depressed conscious level. The urgent ABG will clarify this and give us an immediate lactate level.

Given a blood glucose of 18 mmol/L, I also want an immediate point-of-care capillary ketone check to screen for early diabetic ketoacidosis (DKA). Managing insulin-dependent diabetes is exceptionally difficult for unhoused individuals due to the lack of clean needle storage and refrigeration for insulin.

His hyperthermia introduces further critical differentials:

• Central Nervous System Infection: A fever paired with a depressed conscious level makes acute encephalitis or meningitis a primary concern.
• Post-Ictal State: He may have suffered an unwitnessed grand mal seizure in the street. A major generalized seizure naturally triggers a severe systemic inflammatory response, a profound systemic lactic acidosis, and a transient temperature spike, leaving the patient in a deep post-ictal state marked by hypoventilation.

I am closely monitoring him for subtle signs of subclinical status epilepticus, such as microscopic ocular flickering or repetitive, semi-purposeful finger movements. What did his emergency blood gas and lab markers show?

Host [Dr. Amie Burbridge]: The diagnostic tracking returned the following results:

• Arterial Blood Gas: Lactate is significantly elevated at 6.0 mmol/L. Capillary ketones are high at 1.4 mmol/L. His partial pressure of carbon dioxide (pCO_2) is 6.0 kPa (upper limit of normal), his partial pressure of oxygen (pO_2) is low at 15 kPa despite high-flow oxygen, and his pH is stable at 7.37.
• Hematology & Biochemistry: White cell count is elevated at 14.2 \times 10^9 / L (Neutrophils: 10.4). Hemoglobin is 120 g/L. CRP is elevated at 76 mg/L.
• Renal Function: Sodium is 148 mmol/L, potassium is 4.1 mmol/L, urea is high at 19 mmol/L, and creatinine is severely elevated at 232 µmol/L, confirming an acute kidney injury (AKI).

 [Dr. Ben Lovell]: A lactate of 6.0 mmol/L paired with hyperthermia, tachycardia, and a leukocytosis confirms we must treat for systemic sepsis. I will initiate broad-spectrum intravenous antibiotics immediately, using 1.5 grams of Cefuroxime per our local trust guidelines.

His oxygenation demonstrates a significant ventilation-perfusion (V/Q) mismatch, as a pO_2 of 15 kPa on a 15-liter non-rebreathe mask is remarkably low. We will maintain his oxygen targets between 94% and 98%. To manage his hyperketonemia and hyperglycemia, I will initiate a fixed-rate insulin infusion to safely clear the ketones, adding glucose to his fluids once his levels drop below 12 mmol/L to prevent hypoglycemia. We must also deliver careful intravenous fluid resuscitation for his AKI, insert a urinary catheter to track output, and draw urgent blood cultures.

To address his neurological status, we cannot rule out a central nervous system infection. Given his hyperthermia and low GCS, I will add intravenous Acyclovir to cover herpes simplex encephalitis, keeping a close eye on his renal function since the drug is nephrotoxic.

He is currently too unstable for a safe transfer to an MRI scanner without full anesthetic airway support. Since his unenhanced CT head is clear, I will perform an immediate lumbar puncture right here in the Resus bay to evaluate his cerebrospinal fluid. At a GCS of 13, he should be cooperative enough to remain still for the procedure.

The Synthetic Cannabinoid Crash and Toxicology

Host [Dr. Amie Burbridge]: You have covered sepsis, DKA, and encephalitis, and you are proceeding with a lumbar puncture. But let's look closer at his dilated pupils, severe diaphoresis, tachycardia, and hypertension. Earlier, you mentioned a potential sympathetic toxidrome.

During this case, I contacted the National Poisons Information Service for expert advice. They agreed his symptoms pointed toward a potent sympathomimetic toxidrome. This occurs when a substance triggers a massive surge of adrenaline and noradrenaline, overstimulating the sympathetic nervous system. They noted that while cocaine and amphetamines are classic causes, this specific presentation strongly matched a synthetic cannabinoid overdose, commonly known as "Spice." Have you encountered this much in clinical practice?

 [Dr. Ben Lovell]: To be honest, I haven't seen it frequently in my direct practice; I tend to read about it in public health bulletins more than I see it on the ward. I typically expect sympathomimetic patients to present with profound psychomotor agitation. However, it makes complete sense that a patient who ingested the drug hours prior would present in a late-stage physiological crash.

Host [Dr. Amie Burbridge]: Exactly. I was working in inner-city Birmingham at the time, which faces a significant public health challenge with synthetic cannabinoids, a trend mirrored across many major towns and cities in England, particularly within unhoused and prison populations.

The pharmacology of Spice explains the clinical confusion:

• Full Agonism: Unlike natural cannabis, which acts as a partial agonist, synthetic cannabinoids function as potent full agonists at both the CB1 and CB2 cannabinoid receptors.
• The Biphasic Surge: This full receptor activation triggers an intense, initial sympathetic overdrive. Once that peak subsides, the patient experiences a severe central nervous system crash, manifesting as dissociation, a depressed conscious level, bradypnea, and severe seizure activity.

The latest statistics from 2025 show that roughly 50% of the UK prison population utilises these synthetic compounds. Illicit manufacturers liquefy the chemicals and spray them directly onto paper letters sent into facilities, making them exceptionally easy to smuggle and ingest.

Furthermore, because the chemists continuously alter the molecular structure of the synthetic cannabinoid to evade detection, these compounds rarely register on standard hospital urine drug screens. There is no specific reversal agent; emergency management is purely supportive.

We use intravenous benzodiazepines if they present during the hyper-agitated sympathetic overdrive phase, but we avoid them during a GCS crash outside of an intensive care setting. We must also actively cool them for hyperthermia, track their 12-lead ECGs for dangerous QT interval prolongation, support cardiac myocytes with magnesium, and check a CK to screen for rhabdomyolysis.

What is genuinely frightening is the rise of hidden synthetic cannabinoids. Data shows that one in six vapes confiscated on UK school premises last year were contaminated with synthetic cannabinoids. I have managed young patients who presented acutely unwell after using what they believed were standard commercial vapes, completely unaware they were ingesting synthetic compounds.

We are also seeing a major influx of nitazenes—highly potent synthetic opioids. Illicit suppliers are creating complex polydrug mixtures, blending synthetic cannabinoids directly with synthetic opioids. This means patients present with highly atypical, mixed toxidromes that do not fit standard medical textbook descriptions. If a mixed ingestion is suspected, a trial of intravenous Naloxone is entirely reasonable to reverse any hidden opioid-driven respiratory depression.

Auditing the Cumulative Anticholinergic Burden

 [Dr. Ben Lovell]: That is highly valuable. Working in central London, I need to maintain a high index of suspicion for these evolving synthetic compounds when a patient's physiology doesn't quite make sense. His hyperthermia and dilated pupils were the key indicators of autonomic overdrive.

Host [Dr. Amie Burbridge]: This case completely shifted how I approach toxicology. We shouldn't limit our toxicological reasoning to illicit substances; we must look at the prescription profiles of our older, frail patients. Many routine medications carry a heavy anticholinergic burden that can cause severe, drug-induced delirium or altered mental status.

There are excellent validated calculators online to score a patient's cumulative anticholinergic burden. An acute anticholinergic toxidrome closely mirrors these emergency presentations: patients develop hyperthermia, marked urinary retention, dilated pupils, and acute delirium.

We must closely audit our patients' prescription sheets for common offending agents:

• Tricyclic Antidepressants: Medications like Amitriptyline are frequently prescribed at low doses (e.g., 10 mg at night) for chronic neuropathic pain. Introducing this class to an older adult carries significant cognitive risk.
• Bladder Stabilisers: Antimuscarinic agents like Oxybutynin and Solifenacin, commonly prescribed for detrusor overactivity, carry a heavy anticholinergic profile.
• High-Risk Analgesics: Tramadol carries a notable cholinergic and adverse burden while remaining a largely ineffective analgesic; its use should be heavily discouraged in modern geriatrics.
• Selective Serotonin Reuptake Inhibitors (SSRIs): Even widely used antidepressants like Sertraline carry a mild anticholinergic burden that can act synergistically when combined with other high-risk medications.

When I was a foundation doctor, sending postoperative patients home on a combination of Paracetamol and Tramadol was standard practice. Today, the clinical consensus has shifted entirely; we avoid Tramadol due to its adverse profile. We must look out for the cumulative effect of these everyday prescriptions.

 [Dr. Ben Lovell]: I thoroughly enjoy these complex, urgent cases. It is the absolute core of acute medicine—stabilizing a critically unwell patient while actively solving a complex physiological puzzle. It feeds the clinical soul.

Host [Dr. Amie Burbridge]: I will close today with a famous maxim from the historical physician Paracelsus: "All things are poison, and nothing is without poison; the dosage alone makes it so." He was a pioneer who rejected rigid ancient dogmas, and he was among the first to declare that direct, careful observation of the patient is where the true diagnostic clues reside.

Our key takeaway for this episode is to always consider cumulative anticholinergic burdens, maintain an awareness of modern synthetic compounds, and utilize expert toxidrome lifelines when an presentation doesn't fit standard patterns.

Thank you, Ben, and a massive thank you to our community for listening! Please take a moment to rate, review, and subscribe on your platform of choice. See you next time, and goodbye!

 [Dr. Ben Lovell]: Thank you, Amie. Goodbye!

Clinical Concepts & Pathologies

• Glasgow Coma Scale (GCS): A standardized neurological scale used to objectively assess a patient's conscious level based on ocular, verbal, and motor responses.
• Sympathomimetic Toxidrome: A toxicological syndrome caused by excess adrenergic stimulation, characterized by tachycardia, hypertension, diaphoresis, hyperthermia, and pupillary dilation.
• Anticholinergic Burden: The cumulative effect of using multiple medications with antimuscarinic properties, which can cause delirium, hyperthermia, and urinary retention.
• Diabetic Ketoacidosis (DKA): A life-threatening metabolic emergency characterized by hyperglycemia, systemic metabolic acidosis, and elevated blood ketones.
• Acute Kidney Injury (AKI): A sudden, rapid decline in renal excretory function, marked by a significant rise in serum creatinine and urea.
• Herpes Simplex Encephalitis: An acute, severe viral infection of the brain parenchyma, presenting with hyperthermia, altered mental status, and focal deficits.
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Toxicological & Pharmaceutical Substances

• Synthetic Cannabinoids ("Spice"): Highly potent full agonists at cannabinoid receptors that trigger a severe, biphasic sympathomimetic overdrive followed by a central nervous system crash.
• Nitazenes: A class of highly potent, synthetic illicit opioids frequently mixed into polydrug supplies, carrying a high risk of respiratory depression.
• Amitriptyline: A tricyclic antidepressant frequently used off-label for chronic neuropathic pain; carries a very high anticholinergic burden.
• Oxybutynin / Solifenacin: Antimuscarinic bladder stabilizers used for urinary incontinence; known triggers for drug-induced cognitive decline in older adults.
• Tramadol: A synthetic opioid analgesic with atypical properties; heavily discouraged in modern geriatrics due to its cognitive side effects and poor efficacy.
• Naloxone: A rapid-acting opioid antagonist used to reverse life-threatening respiratory depression caused by opioid toxicity.

What is the systematic diagnostic approach for an unidentified patient presenting with a profoundly depressed conscious level? When a patient presents with an unknown history and a low Glasgow Coma Scale (GCS) score, clinicians must execute an immediate, structured A-E assessment while concurrently ruling out acute intracranial lesions via a CT head, critical metabolic disturbances via capillary glucose checks, and systemic toxicities. If unenhanced neuroimaging is clear, the focus must shift to evaluating physiological tracking patterns like pupillary changes, respiratory rates, and temperature fluctuations to screen for hidden toxidromes.

How do synthetic cannabinoid overdoses physiologically manifest during the late-stage "crash" phase? While synthetic cannabinoids initially trigger an intense sympathomimetic toxidrome marked by hypertension, tachycardia, and diaphoresis, the subsequent physiological "crash" causes severe central nervous system depression, profound bradypnea, potential seizure activity, and a severely diminished GCS. Because these compounds continuously alter their chemical synthesis to evade standard laboratory toxicology screens, diagnosis relies heavily on clinical history and non-judgmental toxicological profiling.

Why is it essential to calculate the total anticholinergic burden in patients with unexplained altered mental status? Many commonly prescribed medications, including certain antidepressants, bladder stabilizers, and analgesics, possess cumulative anticholinergic properties that synergistically disrupt central neurotransmission. An elevated anticholinergic burden can trigger severe hyperthermia, urinary retention, dilated pupils, and acute delirium, necessitating a thorough prescription audit when investigating metabolic or neurological decline.

• – Introduction & Resus Case Launch: Dr. Amie Burbridge presents a classic medical registry puzzle: an unidentified 47-year-old male found unconscious on the street.
• – The 90-Second Heuristic Framework: Dr. Ben Lovell details his rapid mental shortcut checklist for an unknown low GCS, targeting intracranial, metabolic, and toxic axes.
• – Executing the Urgent A-E Assessment: A step-by-step masterclass on airway maintenance thresholds, volume status checks, and managing acute hypoxia.
• – Dissecting the Vitals & Intracranial Status: Analyzing a normal CT head alongside unexpected tachycardia, hypertension, and a respiratory rate of 10.
• – The General Inspection Clues: Exploring the diagnostic implications of an unkempt appearance, diffuse bruising, and a capillary blood glucose of 18 mmol/L.
• – Formulating the Resuscitation Strategy: Balancing metabolic acidosis, early hyperketonemia, and escalating the diagnostic search toward neuro-infections.
• – Sepsis Six vs. Lumbar Puncture: Managing a lactate of six while weighing the logistics of an immediate lumbar puncture against a risky MRI transfer.
• – Demystifying the Sympathomimetic Toxidrome: Evaluating how dilated pupils and hyperthermia point toward massive noradrenaline surges and receptor saturation.
• – The Realities of Synthetic Cannabinoids: Shifting perspectives onto "Spice" and decoding the cellular mechanics, market trends, and prison smuggling profiles.
• – The Threat of Adulterated Vapes: A sobering look at the rising statistics of synthetic cannabinoid contamination on school premises and adolescent public health.
• – Mixed Toxidromes and Synthetic Opioids: Understanding how polydrug use and emerging nitazenes completely mask standard clinical textbook presentations.
• – Auditing the Anticholinergic Burden: Transitioning from illicit toxicities to iatrogenic dangers, unpacking how everyday prescriptions cause profound delirium.
• – Deprecating Tramadol and High-Risk Prescriptions: A critical review of pain management tools, bladder overactivity medications, and antidepressant interactions.
• – Epilogue & The Wisdom of Paracelsus: Closing with a classic historical quote on dosing and celebrating the primary clinical value of direct patient observation.