​Kembara Xtra - Medicine- Carbon Monoxide Poisoning

​Kembara Xtra - Medicine- Carbon Monoxide Poisoning 
Introduction Carbon monoxide (CO) is a gas that is formed when carbon-based substances burn partially. It has no flavor, smell, or color. When inhaled, CO has the potential to be lethal and may result in vague symptoms.
- CO inhalation causes hemoglobin to lose its ability to bind oxygen, forming carboxyhemoglobin (COHb).
– Due to a reduction in oxygen carrying capacity and a shift to the left in the oxyhemoglobin dissociation curve, the production of COHb causes tissue hypoxia.
- CO inhibits the synthesis of adenosine triphosphate (ATP) via binding to mitochondrial cytochrome oxidase. Additionally, it binds to myoglobin and impairs muscular activity.
cardiovascular, pulmonary, musculoskeletal, and neurological system
Pregnancy Considerations
Because CO has a greater affinity and a longer half-life when linked to fetal hemoglobin, tissue hypoxia brought on by CO poisoning may result in serious fetal defects. Therefore, even if the mother is unaffected, the fetus may experience negative effects.

Incidence and prevalence in Epidemiology 

Incidence
The third most common cause of poisoning deaths in the US is CO poisoning.
 Represents 50,000 ER visits each year (16 instances per 100,000 people); 1-3% of these are fatal.
Each year, 15,000 purposeful poisonings take place, accounting for 2/3 of all reported fatalities (10 times more than accidental poisonings).
Causes between 1,200 and 1,600 poisoning-related deaths annually in the United States; Vague symptoms may discourage patients from seeking medical attention, which could result in underdiagnosis.
Prevalence
More often in the winter in regions with a cooler climate
CO poisoning can also result through occupational exposure to methylene chloride, an industrial solvent that is used in paint removal.

Pathophysiology 
Through the lungs, CO is quickly absorbed and binds hemoglobin with 210–240 times the affinity of oxygen.
This reduces oxygen-carrying capacity and delivery, stabilizes hemoglobin in the relaxed high affinity state (R state), and causes a left shift in the oxyhemoglobin dissociation curve.
CO renders cytochrome oxidase inactive. Because of this, ATP synthesis is reduced, particularly in regions like the brain and heart that have high metabolic demands. The electron transport chain keeps going, producing superoxide radicals and causing more harm.
CO displaces NO from platelets, causing platelet activation and aggregation; increased peroxynitrite production contributes to reduced mitochondrial function and hypoxia; increased peroxynitrite production. Additional impacts include apoptosis, lipid peroxidation, and oxidative stress.
Hypoxia and mitochondrial failure cause myocardial shock and damage.
Xanthine oxidase is created when xanthine hydrogenase interacts with proteases produced during neutrophil degranulation. Endogenous protection against oxidative stress is inhibited by this.
Further ischemia is caused by excitatory amino acid synthesis in the brain, increased nitrite levels, and an inflammatory cascade that can result in delayed neurologic impairment and oxidative destruction of nervous system lipids.
Additionally, CO encourages the release of NO, which can result in severe hypotension.

Risk factors include: drinking and smoking; patients with severe COPD, independent of recent exposure to tobacco smoke; enclosed or inadequately ventilated spaces; fires and injuries caused by fires.
High-risk occupations include auto mechanics, paint strippers, solvent industry workers, and those who work around faulty furnaces, stoves, generators, and other fuel-burning devices. If exposed, infants, the elderly, and people with comorbid conditions like cardiovascular disease, anemia, and chronic respiratory conditions are at a higher risk of experiencing negative outcomes.


Limiting occupational exposures for those who work with cars, paint, solvents, or mines. Prevention. Installation of in-home CO monitors or alarms. Postexposure determination of CO source to limit future exposures, eliminate source, and begin treatment. Public policy to ensure building code safety.

Accompanying Conditions 

Following smoke inhalation, CO and cyanide poisoning frequently happen simultaneously and have additive effects.

 About 40% of the time, intentional poisoning happens in conjunction with the absorption of other substances.
Up to 50–75% of fire-related injuries include CO poisoning as a factor.

What is a diagnosis?
Clinical triad of increased COHb levels, history of CO exposure, and pertinent symptoms
Exposure is proven by an elevated COHb level of >3% in a nonsmoker and >10% in a smoker. The COHb level is required for the diagnosis even if it has no relationship to the illness's severity or long-term outlook.

Older pulse oximeters cannot distinguish between oxyhemoglobin and COHb, giving a hypoxic patient normal oximeter results. Eight-wavelength CO oximeters are able to identify CO exposure, but they are unable to accurately identify CO poisoning.


The duration and mechanism of exposure are key factors in the diagnosis of CO poisoning. There is no one sensitive or particular sign. A high degree of skepticism must be maintained.
The following are typical signs:
Pain in the head (84% of patients)
- Disorientation/poor judgment
- Vertigo
- Vomiting/nausea
- Tiredness
- Aches and pains in the chest; wheezing
Patients may also have syncope, seizures, visual abnormalities, arrhythmias, and loss of consciousness.
● Some patients may exhibit cardiopulmonary symptoms as shortness of breath, palpitations, or chest pain.
Repeated exposure to low CO concentrations causes long-term (subacute) exposure, which is defined as >24 hours. Chronic weariness, emotional anguish, memory loss, difficulty concentrating, sleep difficulties, vertigo, neuropathy, recurring infections, polycythemia, paresthesia, abdominal pain, and diarrhea are among the symptoms.
Exclude all female patients who are pregnant.

clinical assessment

The distinction between oxygenated hemoglobin, deoxygenated hemoglobin, COHb, and methemoglobin is not made by pulse oximetry. Therefore, blood gas analysis using a co-oximeter to quantify COHb levels in individuals exposed to CO is required.
Results can vary. Patients frequently complain of bewilderment or altered mental state.
Skin and lip colors that are traditionally classified as "cherry red" are uncommon (around 1% of occurrences).
Inspect for evidence of secondary injuries, such as skin and oropharynx burns (caused by flames in enclosed spaces).
Full neurologic and mental state evaluations; ataxia, visual field abnormalities, papilledema, and nystagmus; as well as confusion/CNS depression
Tachycardia, hypotension, and cardiac dysrhythmias are also present. Respiratory depression or tachypnea and cyanosis
Pulse oximetry can be deceptive, as was previously mentioned.

Differential Diagnosis: Methylene chloride (dichloromethane) inhalation or ingestion; Cyanide Toxicity (also Co-Existing); Viral Syndromes
Meningitis or encephalitis; metabolic factors (hypoglycemia, electrolyte imbalance); alcohol intoxication; opiates; acetylsalicylic acid (ASA) overdose; behavioral problems (major depressive disorder); trauma; CNS lesions; and concurrent use of another drug.

Diagnostic tests and laboratory results 
Initial examinations (lab, imaging)
A recent history of CO exposure, recurring symptoms, and evidence of a high COHb level are all necessary for diagnosis.
Chronic CO poisoning is more challenging to identify because there isn't a distinct triggering event.
It is not recommended to utilize non-invasive COHb monitoring to identify CO poisoning.
It's advised to get an arterial or venous blood gas:
- COHb values in smokers of >10% and non-smokers of >3%.
Despite severe poisoning, COHb may be low (for example, if O2 therapy is administered or if a large amount of time passes before the level is obtained).
- Severe metabolic acidosis; anion gap greater than 16
- A higher lactate level indicates a worse prognosis.
- Because O2 dissolved in blood is unaffected by CO, PaO2 often remains normal.
Basic labs: CBC and serum chemistries
ECG for every patient
- Cardiac enzymes in victims of severe or mild poisoning. All patients have an elevated risk of mortality (24%), and the risk is substantially higher in the following populations (2)[B]:
Patients under 65 years old, those with cardiac risk factors, and those who are anemic
 Signs and symptoms of cardiac ischemia

All women who are fertile should get tested for pregnancy, and toxicology screenings are crucial in cases of purposeful poisoning.
Head CT/MRI scans can help rule out alternative neurologic reasons and may also show an infarction caused by hypoxia or ischemia. CK is used to test for rhabdomyolysis. Hippocampal atrophy and persistent white matter hyperintensities also take place.

Tests in the Future & Special Considerations
Consider CO poisoning in younger patients who have chest discomfort or other ischemia-related symptoms.
Consider the diagnosis in patients who are afebrile and have nebulous or "flulike" symptoms. Both CO poisoning and the flu are prevalent in the winter.
Patients with purposeful poisoning should receive behavioral examination when stable since they may present as a group (coworkers, family members, or schoolchildren) with identical symptoms.
If necessary, take safeguards against suicide.


Management Treatment Intubation and mechanical ventilation may be required for severe intoxication, particularly if the patient is unable to protect their airway or if there are signs of respiratory failure. Prompt removal from the CO source and initiation of oxygen therapy to displace CO. Supportive care as necessary.


Regardless of oxygen saturation or PO2, administer 100% oxygen via a non-rebreather reservoir facemask until COHb is normal (3%) and the patient is symptom-free. CO has a half-life of 250–320 minutes in room air, but this half-life is decreased to 90 minutes with oxygen therapy.
Hyperbaric oxygen therapy in second line (not always accessible)

Further Treatments 
Although the requirements for beginning therapy are still unclear, hyperbaric oxygen (HBO2) is linked to lower long- and short-term death rates as well as long-term neuropsychiatric problems.
The elimination half-life of COHb is shortened by NBO2 and HBO2 to 85 and 20 minutes, respectively.
If HBO2 is not available, inject NBO2 until symptoms disappear and CO returns to normal.
HBO2 therapy can reverse mitochondrial malfunction and the inflammatory response, which can help to lessen long-term neurologic deficit.
Uncertain HBO2 protocols exist.
Currently, HBO2 is advised for the following conditions: >24-hour exposure; levels >25%; pregnant patients with CO levels >20%; loss of consciousness; abnormal neurologic or psychiatric symptoms; cardiovascular failure or end organ ischemia
Serious acidosis 
If the pH is 7.20 or the plasma lactate level is >10 mmol/L, empirically treat patients who report with CO poisoning from a house fire for cyanide poisoning.
HBO2 is less likely to be beneficial if more than 24 hours have passed since exposure. The greatest benefit is experienced when treatment is started as soon as feasible, ideally within six hours of exposure.
Expert opinion generally supports HBO2 therapy for expectant women.
Patients should be taken to the closest HBO2 facility if their symptoms do not improve after 4 to 5 hours on 100% oxygen. Patients with acute poisoning, ECG or lab evidence of end-organ damage, and those with worry-inspiring medical or social circumstances should be hospitalized.
After intubation, transfer unconscious CO poisoning patients to the intensive care unit.
Patients who suffer from accidental poisoning and have minor symptoms that go away in the ED can be released without risk.


Follow-up: One to two months after being discharged, all patients who underwent treatment for acute CO poisoning should return.
Seek neuropsychological examination if there are any behavioral or cognitive issues, especially after deliberate CO poisoning.
It can be necessary to undergo long-term cognitive, psychological, speech, occupational, and physical rehabilitation.
patient observation
Repeated arterial blood gas measurements of COHb levels.
 Installation and upkeep of combustion devices by qualified personnel CO detectors in bedrooms and around potential CO sources

 Annual checks of the furnace
Prevent using combustion engines indoors, and perform regular furnace inspections

 Prognosis
Despite the fact that the majority of patients fully recover, 12–68% of individuals report having chronic neuropsychiatric disability.

Complications 
The danger is greater for tissues with high metabolic activity.
Cardiac: Acute and chronic myocardial infarction
- Ischemia on demand
- Decreased left ventricular performance
- Prolonged QT (dysrhythmia)
Pulmonary: - Pulmonary edema - Inhalation injury
- Aspiration pneumonia - Acute respiratory failure
Neurological: motor and vestibular impairments as well as anoxic encephalopathy
Cognitive impairment, Parkinsonism, delayed posthypoxic leukoencephalopathy, diffuse brain atrophy, hippocampal atrophy
Behavioral: irritability, moodiness, aggression, and depression and anxiety
Aspects of Geriatrics
An increase in comorbid conditions increases the likelihood of complications and worse results.