Hypothermia and ecg changes

Hypothermia:

Hypothermia is defined as body temp below 95 F or 35 C + altered mental status and neurodeficit (i.e. Ataxia)

Hypothermic heart is prone to arrythmias, incl V fib

Importently ::: most acurate way to determine a patients temp is via Esophageal thermometer (better than rectal or bladder) !!!

Cold Stress:

Something hypothermia do to the system:: We can say it as Cold stress

Cold stress>> Slowing of Physiologic functions (metabolism, enzymatic reactions)>> it will result in 2 things

1.. Decreased automaticity

2. Decreased Conduction ability of cardiac tissue

1 & 2 >> will lead to conduction delay

As a result of this mechanism> Related ECG findings will be found as in the above case i.e: PR prolongation, QRS widening, Bradyarrythmias, J (OsBorn) wave, irregular baseline (shivering induced)

Difference between STE and J wave is given in this picture

Next Question comes in mind, what are the major Culprits in Hypothermia

There are few::

1. Heat Loss (accidental cold exposure may be ;)

2. Vasodilation: - Drugs, -Alcohol, - Sepsis

3. Impaired Heat Production: -Endocrine disorder, - malnutrition, - Hypoglycemia

4. Iatrogenic: -Massive Transfusion, - Dialysis, -Intentional Hypothermia protocol goes wrong

5. Impaired Thermoreglation:: -SPinal cord injury, - CVA, Hypothalamic injury

Now i am going to explain some pathophysiology and hemodynamics in Hypothermia

Initially there will be increase in SVR via vasoconstriction to prevent heat loss and maintain core temperature.

This will result in increased central blood volume>> causing an inhibition of ADH release>> resulting into large quantities od dilute urine (cold induced Diuresis)>> resulting into HYPOTENSION

This cold results into these changes above, so while treating these patients we should be careful as our patient may need/ has>> Labile Vital Signs (possible pressor needs), Fluid requirements accordingly

Credits: IMCore

I hope we learnt today something. More facts to come soon

How chloroquine will act as a prophylactic drug and is acting as a therapeutic agent against COVID-19 infection

*How chloroquine will act as a prophylactic drug and is acting as a therapeutic agent against COVID-19 infection.*

Chloroquine acts on host target respiratory cells by:
Chloroquine increases the endosomal pH required for the virus- host target cell fusion. Increase in the pH disrupts the normal viral function.
In SARS-coronavirus, which is a sister to COVID-19, chloroquine was found to interfere with the glycosylation of cellular receptors of the virus. This interference eventually resulted in no association between the host target cell and the virus.
Chloroquine acts as an ionophoric agent for Zinc ions and thus increases the in flux of zinc ions into the cytoplasm of host target cells regardless whether the host target cells are infected or not.

All the above-mentionedgas mechanism is on the host cells and COVID-19 can not mutate and cause resistance to these 3 mechanisms. First 2 mechanisms inhibit the virus-target host cell union. Chloroquine results in disablement of ACE2 (Angiotensin converting enzyme 2) terminal glycosylation which leads to the morphological change; ACE-2 is a surface receptor found on target host cell. This results in the disruption in the association between the COVID-19 and target host cell as COVID-19 requires ACE-2 receptor to attach to a cell.     
Because the action is on the target host cell, Chloroquine won’t develop resistance therapeutically. If a person uses Chloroquine as a prophylactic agent (500mg once in a week for adults and 8.3 mg per kg once in a week for children) against COVID-19 then, it will act pre-infection and post-infection. If a person does not get exposed to the COVID-19 infection after taking Chloroquine (say for 3 weeks) and then some viruses enters and try to infect target host cells, Chloroquine mechanism “a” and mechanism “b” will prevent the union of virus-target host cell. If some of the viruses enters the target host cell, there Zinc ions are waiting to adhere to the RNA dependent RNA polymerase enzyme of the virus and stops COVID-19 polymerization intracellularly. If COVID-19 mutates inside the cell several times, even then the Zinc ions will actively inhibit the viral multiplication inside the host respiratory cells, irrespective of the viral strain. Even if COVID-19 virus manages to escape from Zinc ions trap and releases from the host target cell cytoplasm into the interstitial matrix, intercellular space, and tried to re-infect some of the healthy target host cells, Chloroquine will prevent the re-union of viral genome with target host cells via mechanism ‘a’ and mechanism ‘b’ and the infection will halt in the preliminary stages itself and complications like COVID-19 pneumonia will not develop. Chloroquine molecules will not lose its effectivity in an individual pre and post infection.
Zinc is present in ample amount in the human body. In normal conditions, the Zinc is not present in free state in the cell. The increased level of Zinc ions is not toxic to the cells and cells excrete the extra Zinc ions into the extracellular space. Zinc is commonly present in red meat, legumes, nuts, milk, cheese, eggs, whole grains etc. Garlic increases the absorption and bioavailability of Zinc inside the body. So, some persons who aren’t taking Zinc rich foods in ample amount should eat zinc supplements or garlic daily. 

Safety of Chloroquine is well tested as it is given for
Malaria prophylaxis
Autoimmune diseases like rheumatoid arthritis
Lupus erythematosus
Now a days it is indicated into the SARS infection as it is a broad antiviral agent.
Through it ionophoric action for its zinc intracellular influx, chloroquine is also used as anti-cancerous drug.

The long-term use of chloroquine (4 years together) may cause its accumulation in the eye. There are some concerns of its use in glucose-6-phosphate dehydrogenase enzyme deficient children but the recommended prophylactic and therapeutic doses, Chloroquine is safe to be used in these children. Some persons may complain of acidity and nausea, but it can be resolved if Chloroquine is taken post meal.





Prophylactic dose in malaria is 500 mg once a week in adults and 8.3 mg per kg once a week in children.
In these doses it will be effective against COVID-19 prophylaxis. The therapeutic doses against COVID-19 as used in China, America and India are Chloroquine 500mg BD for 5 days with other anti-viral drugs like Oseltamivir, Lopinavir, Ritonavir etc. and in complicated COVID-19 pneumonia cases, Chloroquine may be used for 10 or more days in the same amount.

Now comes the actual catch of its technicality to be used prophylactically against COVID-19 action. In India as it is a very cheap, safe and easily available drug and can be prescribed against the Malaria as a prophylactic drug as the summer season approaches. It will surely work prophylactically against the COVID-19 outbreak and we can use this opportunity to prescribe it in larger amount as Malaria is endemic in India. It will act on Malaria and COVID-19 infection prophylactically without it being included in the guidelines.
Trump’s excitement for chloroquine in his announcement can be related with the fact that American researchers are currently working on the Chloroquine drug. Many companies have donated chloroquine to the US for research purpose.
Hydroxychloroquine is less toxic but original Chinese work is based on chloroquine phosphate. Hydroxychloroquine can be used with equal efficacy.
If one starts prophylactically with Chloroquine, then one must stick with chloroquine and must not switch to hydroxychloroquine and vice-versa. This switch may result in increase QT interval.

*REFERENCES*
Zhu N, Zhang D, Wang W et al. A novel coronavirus from patients with pneumonia in China, 2019. N Engl J Med 2020
Gao, J., Tian, Z. and Yang, X., 2020. Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies. BioScience Trends.
Vincent, M., Bergeron, E., Benjannet, S., Erickson, B., Rollin, P., Ksiazek, T., Seidah, N. and Nichol, S., 2005. Virology Journal, 2(1), p.69.
https://youtu.be/U7F1cnWup9M






SARS-CoV-2 RNA more readily detected in induced sputum than in throat swabs of convalescent COVID-19 patients - The Lancet Infectious Diseases
https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30174-2/fulltext

‏LABORATORY MARKERS IN COVID-19

‏LABORATORY MARKERS IN COVID-19 PATIENTS :microscope::syringe:
‏MOST FREQUENT
‏Decrease lymphocyte count
‏Decrease albumin
‏Decrease hemoglobin levels
‏Increase C-reactive protein (CRP)
‏Increase Erythrocyte Sedimentation Rate (ESR)
‏Increase Lactate Dehydrogenase (LDH)
‏Increase D-dimer

- Deaths from Covid-19 are due to (1) cytokine storm syndrome and (2) fulminant myocarditis.

- During a cytokine storm, an excessive immune response ravages healthy lung tissue, leading to acute respiratory distress and multi-organ failure.

- All Covid-19 patients sick enough for hospitalization should be given a serum ferritin blood test.

- Elevated serum ferritin values are a good first screening tool for the possibility of a cytokine storm syndrome in sick patients with high fevers.

- Treating Covid-19 infected patients with cytokine storm syndrome with IL-6 blockade (tocilizumab) has recently been reported in China with successful outcomes.

- Fulminant myocarditis :heart: has also been reported in patients with Covid-19

- Fulminant myocarditis is primarily caused by infection with viruses. It arises quickly, progresses rapidly, and may lead to severe heart failure or circulatory failure presenting as rapid-onset hypotension and cardiogenic shock, with mortality rates as high as 50%–70%.

- Physicians should pay attention not only to the symptoms of respiratory dysfunction but also the symptoms of cardiac injury.

_\\\\______
‏Source: Lippi G, Plebiani M. Laboratory
abnormalities in patient with COVID-19 infection. Clin Chem Lab Med. 2020 Mar 3. doi: 10.1515/cclm-2020-0198 Covid-19 🦠 Update:*

Current criteria to swab for COVID-19

Current criteria to swab for COVID-19 in the UK:

Clinical : Pneumonia clinical or radiological, ARDS, Flu like illness (fever, cough whether productive or non productive, sore throat, runny nose, myalgia. Less people present initially with diarrhea 10% and they had the worst prognosis later from the Wuhan experience)
Or Epidemiological : last 14 days in tier 1 or tier 2 countries. Or contact with confirmed case of COVID-19.

-Incubation period 4 - 14 days. People are infective mostly in the first 5 days when the symptoms are milder. Deterioration happens after day 10 of the symptoms (when the body enter into the adaptive immunity stage)

-PCR for COVID19 sensitive for 70% only, may be initially negative, a repeat PCR in high suspected cases recommended in 48 -72 hours.

-CT Thorax is sensitive for 97% of cases and could help in diagnosis of patient with initial negative PCR (positive CT Thorax for COVID-19 is patchy ground-glass appearance in the lung peripheries, it does not cause cavitation or lymphadenopathy)

- Old age >70, High SOFA score, and d-dimers >1000 are risk factors for poor prognosis.
Pediatrics guidelines if needed please contact me freely and i will provide you details with evidence.

-Lymphopenia with normal WBC count is common in 80%, mild thrombocytopenia , high CRP and ferritin tract with disease severity.

-High tropronin found in half of the dead patients (perhaps as IHD was a common risk factor, likely it is troponin leakage form sepsis /strain? some reported cases for severe myocarditis). Considered as a marker for poor prognosis.

-Give empirical antibiotics in the golden hour as per the normal sepsis protocol . Blood cultures./Procalcitonin. Review ABX in 48 hours.
-NO IV Fluids, unless there is an evidence of hypo-perfusion.
-No role of steroids as it delays viral clearance, unless the patient has obstructive airway disease or Septic shock not fluid or vasopressor responsive

-Controversial role of Hydroxychloroquine: it interfers with cellular ACE receptors in the lung, hence has some anti-viral activities.

-Some Antiviral therapies like Remdesivir, combination of Lopinavir/Ritonavir/Ribavirin is of benefit in MERS, no evidence of use it in COVID-19, Clinical trials are taking place currently. If the patient deteriorated, consider them after discussion with the local ID team. No role of using Oseltamavir in COVID-19 unless influenza is considered when you admit the patient.

- Cytokines storm inhibitors in COVID-19: as the disease cause a cytokines storm (elevated inflammatory markers like CRP, ESR, ferritin), selective inhibition of cytokines Tocilizumab showed some benefit in phase 3 RCT in China. The drug was eventually licensed in China for severe COVID-19 infection.

- COVID-19 may cause secondary HLH?

-Severe respiratory failure/?ARDS: ITU for early Intubation and ventilation with low TV and allow for permissive hypercapenia, prone, paralysis, APRV, ECMO.
(HFNO and NIV is not recommended)

-Cardiac arrest in COVID-19:
Identify resuscitation status for any ?COVID-19 hospital admission.
Recognize cardiac arrest by absence signs of life and absent carotid pulse. Do not do listen and feel for breathing.
Wear full PPE (FFP3, Visor, Gloves, plastic apron) then start CPR. The likely cause is a hypoxic arrest. However, the recommendation from resuscitation council UK is to start with CRP. Early ventilation is advised.

Evaluation of Pseudocoma VS Coma

Evaluation of Pseudocoma

Difference Pseudocoma VS Coma

Here is a short table to quickly differentiate a patient with pseudocoma from true coma

How to approach an unconscious patient in Emergency Department

How to approach an unconscious patient in Emergency Department:

One of the most challenging approach is to an unconscious patient presenting to emergency department. An emergency physician needs to keep him/herself gathered to approach a patient like this; in order not to miss a life threatening condition in a silent patient.

The 4 core components of care, history, examination, investigation and treatment should go in parallel. A systematic & structured approach should be employed by teams caring an unconscious patient i.e. ABCDE (Airway, Breathing, Circulation, Disability, Exposure), Vital signs, CPR, Intubation or Oxygen?, Blood samples, To give Glucose and/or Thiamine, History, Examination & Observation, etc

All steps should be followed simultaneously giving importance to TIME.

Time Constrained Approach:

'Time is Brain, Time is Heart'

What can kill the patient first?
Initial thought is 'How to make the patient survive next few minutes' then 'Further Minutes of survival' and then 'Hours' and 'To survive this event'.

Within First Minute:

First thing first:

Simultaneously Assess for:

1. Cardiac Arrest: Check Pulse
2. Airway: While checking pulse, assess airway patency and look for any Foreign body if obvious
3. Breathing: Pattern of breathing

All these things will be ongoing while the nurses are doing the vital signs and connecting to the cardiac monitor/defibrillator. Also accessing 2 IV lines and extracting blood.

Lets take it here: 

1. If cardiac arrest>>>> Proceed to Basic life support and start CPR

2. Airway & abnormal breathing>>>Assisted ventilation / Intubation (Intubate if necessary to protect airway)

What next to do:: 

Very Important part of Vital sign is:

Blood Sugar>>>> check for hypoglycemia, it should never be overlooked

If Hypoglycemia: treat hypoglycemia with:

-Inj D50% 50ml 1-2 Ampoules IV 

Patient of hypoglycemia be:

1. Low blood sugar 2.8 to 3.0 Mmol/dl or 50 to 54 mg/dl
2. Return to usual state after Dextrose bolus
3. No residual deficit

The above 3 point should be there to determine if all the symptoms of patient were due to Hypoglycemia

What else can Kill patient in next few Minutes:

-Drug overdose

-Intracranial Hypertension

While assessing these, simultaneous quick survey is important.

Assess for:

• Signs of Shock: Capillary Refil/Cold or Warm Skin
• Neuro: Check Pupils, Eye movements, Corneal reflex, moving all 4 extremities, any asymmetry?
• Toxidrome: Pupils, Vital Signs, Skin
• Breathing Pattern: Regular, Irregular
• Abdomen: Any signs of Pulsating masses, Pain?
• Chest: Any sign of tension Pneumothorax, deformity?
• Trauma: Any obvious deformity or trauma?

Toxidromes: 

• In case of Opioid toxicity: Inj Nalaxone 0.2-0.4mg IV, start at lower doses if patient is stable to avoid precipitating rapid opioid withdrawal.
• Wernicke's ncephalopathy: Inj Thiamine 100mg IV

Signs of impending herniation: Intubate; provide analgesia and sedation; elevated the head of the bed; respirate to a target pCO2 of 35mmHg; Mannitol 0.5-1gram IV or 3% hypertonic saline 2-3ml/kg IV bolus.

What else should be done simultaneously:

Always remember H & T's of ACLS

H(HYPOGLYCEMIA, HYPERKALEMIA, HYPOTHERMIA, HYPOXIA, HYPOVOLEMIA, HYDROGEN ION(Acidosis)

T(Toxins, Tamponade(cardiac),Tension pneumothorax, Thrombosis (coronary and pulmonary), and Trauma)

• ECG: check rate, abnormal rhythm, look for Ischemia, Hyperkalemia (Confirm by STAT VBG) (be prepared for Pacing/Defibrillation)
• Portable Chest X ray: Hemo/Pneumothorax
• Bedside U/S: RUSH Exam

What Can threat patient's Life here:

• STEMI: Stabilize patient, Cath Lab activation
• Pulmonary Embolism: Tachycardic, Hypotensive, Sob, Arrested> Thrombolysis, Deteriorating patient>thrombectomy
• AAA: Stabilize and early involvement of Vascular / Cardiology/ Critical Care specialist
• Tension Pneumothorax: Needle decompression via large bore in 2nd intercostal space midclavicular line
• Hypotension: Start IV fluids/ blood products according to context
• Anaphylaxis: Inj Epinephrine 1:1000 (each ml contains 1mg of 1:1000) intramuscular should be given with following dosage
• Age More than 12 years/ Adults:  0.5mg (500mcg) IM (0.5ml of 1:1000 solution)
• Age 6-12 years: 0.3mg I/M (0.3ml of 1:1000 solution)
• Age 6 Months to 6 years: 0.15mg IM (0.15ml of 1:1000 solution)
• Less than 6 Months: 0.01mg/kg IM (0.01ml/kg of 1:1000 solution)
• Hyperkalemia: Inj Ca-Gluconate 10% of 10ml over 10min (equal to 1gm of calcium gluconate), Prefer Inj Calcium chloride in patients with cardiac arrest instead of calcium gluconate because the chloride formulation has approximately 3 times the amount of elemental calcium compared with the gluconate formulation.
• Treat Seizures with anticonvulsants
• Consider Encephalitis if altered LOC with fever history and start Acyclovoir

What else?

After initial approach so far which an emergency physician completes within 10-15min simultaneously managing appropriately, there are wide differentials to get lost in.

Stay systematic and think of further differentials which can pose risk at patient's life:

• Hypertensive emergencies/ Intracranial hemorrhage 
• Delirium Tremens/ withdrawl
• Infection like Necrotizing fasciitis: Look for sites of infection
• Metabolic disorders like DKA, HHS, severe hyponatremia
• Addisonian's Crisis
• Myasthenic Crisis

Stablize, Stabilize, Stabilize

Before shifting patient to Radiology department for CT Brain

Look for further differentials :

Mnemonic which is easy to remember

AEIOU TIPS

GCS

Evaluation of Pseudocoma Table can be seen here

How to approach a patient with headache in ED

How to approach a patient with headache in ED

A 30 year old patient comes to the emergency department with history of headache.

How to approach this patient in ED & what important points needs to be evaluated in this patient.

Approach:

-Place the patient on automated BP monitoring ,ECGmonitoring& pulse oximetry
-Vital signs: temperature, blood pressure, pulse, and 02 saturation

Detailed History:

High risk patients:

o Age >50 years, with a new or worsening headache
o Sudden onset of worse severe headache in the life (raises concern for subarachnoid
hemorrhage).
o History of head trauma (even in the last 2 weeks)
o Associated symptoms as:
o Fever, neck stiffness, vomiting and photophobia (raises concern for meningitis)
o Fever and behavior changes (raise concern for encephalitis).
o Confusion, Convulsion or Neurological deficit (raise concern for: stroke or, brain
tumor)
o Vertigo or ataxic gait o Visual changes: Specify _
o Change in headache quality, or progressive headache worsening over
weeks/months
o Medication History (warfarin, and antiplatelet agents) (increase the risk for
intracranial hemorrhage)
o Medication history (chronic steroids or immunosuppressants drugs) (increase risk
of CNSinfections)
o Medication history of oral contraceptive pills (increase risk of venous sinus
thrombosis)
o Pregnant Women: Preeclampsia should be considered in pregnant women after
20th week
o Venous sinus thrombosis should be considered as a cause of headache during
pregnancy, the postpartum state, and hypercoagulation state as (SLE,vasculitis)

Low risk patients:

o Facial pain (raise concern of sinusitis or dental infection)
o Temporal area pain increase with jaw movement (raise concern of temporal
arteritis)
o Medical history as uncontrolled hypertension associated with hypertensive
urgency
o Medication history of nitroglycerin or carbon monoxide poisoning
o History Use of cocaine, amphetamine, and alcohol
o Prior Headache History suggestive of migraine, tension, or cluster-type headaches,
and response to specific therapy
o Family History of aneurysm or sudden death in first-degree relatives (raises the
suspicion for intracranial aneurysm)

DETAILED EXAMINATION:

o Complete Neurologic Examination includes:
o Mental status assessment
o Speech
o Gait
o Pupillary examination (for asymmetry or ptosis)
o Cranial nerve examination
o Motor examination to detect extremity weakness
o Deep tendon reflex examination
o Coordination testing (to detect cerebellar lesions)
o Examination of the Eye: to exclude angle-closure glaucoma or 3rd cranial nerve palsy
o Examine the ears, nose, and throat to identify otitis media and sinusitis
o Examination of the Head and Neck: Meningismus is an important clinical clue to
Meningitis.
o Palpate for tenderness over the temporal arteries to assess for possible temporal
arteritis

Important Differential Diagnosis to consider in ED

1. SUBARACHANOID HEMORRHAGE (SAH)
Following are strongly and reliably associated with SAH

• Sudden onset of headache
• Maximal at onset
• Hx of recent similar headache (Sentinel bleed)
• Age >40
• Neck Stiffness or pain
• Onset of headache on exertion
• Vomiting
• Witnessed loss of consciousness
• Elevated Bp of > 160/100

Also consider the following symptoms

• Stroke like symptoms
• Seizure
• 3rd Cranial Nerve palsy from mass effect
• 6th Cranial Nerve Palsy with diplopa
• Subhyaloid Hemorrhage (Terson Syndrome: Dense red on fundoscopy)
• Meningismus

Risk factors:

• Family history of Cerebral bleed
• History of SAH
• Family history of Polycystic kidney disease
• Collagen vascular disease
• Hypertension
• Binge Drinking
• Use of cocaine or smoking
• Onset of headache during exertion
• Presyncope or syncope with headache

Workup of SAH:

ECG::

• Changes occur in 50-100% of patients due to neurogenic myocardial stunning or coronary vasospasm.
• 
Deep,
wide 
precordial 
T‐wave 
inversion,
 bradycardia,
 and
 prolonged
 QT
• Imp::; don't anticoagulate these patients considering the above findings as ACS

CT Brain:

• Sensitive 95% within 12 hours
• Sensitive 85 % after 1 day
• Sensitive 50% after 1 week

Lumber Puncture:

• Lumber puncture is still standard. However 25% are at increased risk of Post LP headache, Infection and neurological damage.
• Important points to consider for LP here as per recommendations:
• Don't wait till 12 hours after onset for Xanthochromia to be reliably present as then the patient will also be at risk of fatal bleed.
• True positive tap may be hidden in Traumatic tap, so if you wanna say it a true negative tap only if RBC are <5 in tube 4 or a decrease in 25% of RBC from tube 1 to 4.
• Opening pressure should be done as it may be elevated in SAH but will not rise in Traumatic tap, can rise in BIH, CVT
• Post LP headache classically occurs day 3 and are worse when not suppine, are result of CSF leaking from dura or it can be called post dural puncture headache PDPH, which is not shown to be helped with bed rest or caffeine intake but only by Blood patch of patient's own blood. Post LP headache can be minimised by use of smaller needle like 25G and using non cutting needles. (By Dr. Anton)
• If unsuccessful LP or refused by patient then do CT angio to find out if any aneurysm identifiable

Management of SAH:

• Involve Neurosurgeon to consider the target BP if MAP is more than 100-110
• To prevent rebleed treat hypertention if MAP is more than 100 to 110 for few hours and can use IV labetolol 20mg iv bolus then 1-2mg/min infusion not to exceed 300mg or 40-80mg iv q10min with blood pressure monitoring every 5-10min. No dosage alteration in renal or hepatic impaired patients been recommended.
• Oral Nimodipine 60mg p/o or Per NG to prevent vasospasm and subsequent cerebral infarct, every 4-6 hours , should be started within 24hours of presentation. It comes in 30mg gel capsules or 30mg/10ml or 60mg/20ml oral solution. Dosage should be decreased to 30mg in hepatic impairment, closely monitor BP (decreases BP) and HR(arrhythmia).
• Consider starting anti-epileptic which can occur in SAH patients

2. MIGRAINE:

Beware of self diagnosis brought in by patient.

To diagnose as a case of Migraine patient should be diagnosed by physician with history of recurrent similar symptoms with similar intensity and character.

Classical Migraine history will be as follows and can be remembered by Mnemonic of POUND

• Pulsatile quality headache, 4-72Hours duration onset, Unilateral pain, Nausea and Disabling intensity of headache. Can be associated with phono and photophobia. 4 out of 5 features are usually present in POUND Mnemonic.
• Can also present with bilateral colored tunnel vision instead of unilateral flashes and floaters white in color and like a black curtain falling down in cases of vitreous and retinal detachment respectively.
• SSNOOP 
mnemonic
 for 
red 
flags:
 Systemic
 signs
 (fever,
 weight
loss),
 Secondary 
risk
 factors
(immuno‐ compromised 
status,
 HIV),
 Neurological
 signs 
(speech 
deficit,
 cranial 
nerve 
abnormalities),
Onset
–
abrupt,
 Older
age
(>40yo),
Progression
 of 
symptoms (By Dr. Lucas)

Management::

• Inj Metoclopramide 10mg IVI slow infusion over 15-20min or inj prochlorperazine over 15min IVI
• Inj Diphenhydramine 50mg IVI in case of development of extrapyramidal symptoms
• Inj Dexamethasone 10-15mg IV or P/O on discharge (to prevent rebound 72 hrs headache) 
by
decreasing 
the 
inflammation 
of
 the 
blood 
vessels 
in 
the 
brain.
• Naproxen 500mg on discharge shown to be equal effect of Triptans (reported to cause chest tightness), give to people who don't have CVS disease.

3. SPONTANEOUS CERVICAL ARTERY DISSECTION:

Cervical artery dissection is a tear in cervical artery (carotid or vertebral artery) with development of intramural hematoma resulting in stenosis, occlusion or aneurysmal dilation.

Cervical artery dissection usually occurs with minor trauma such as hyperextension of neck during shaving, while driving checking upon blind spot, roller coaster ride, boxing or even coughing in case of connective tissue disease.

Evaluation:

Classic Triad of Carotid Artery Dissection: although only 1/3 of patient present with all 3

• Unilateral pain of head, neck or face
• Partial Horner Syndrome (ptosis, miosis)
• Cerebral or retinal ischemia or TIA symptoms

Dissection of Vertebral artery:

• May present with posterior neck pain
• Headache
• Vertigo
• Ataxia
• Swallowing difficulty

Diagnosis is by:

• CT angiography
• Duplex Scan
• MRA

Management:

• Antithrombotic therapy for at least 3-6 months for a patient with ischemic stroke or TIA
• Endovascular stenting
• Surgical Repair

4. Cerebral Venous Sinus Thrombosis:

Can present in young patients, women more than men.
Symptoms can range from:

• Headache (thunderclap to subacute)
• Seizure
• Stroke like symptoms
• Papilledema, orbital chemosis, proptosis

Risk Factors:

• Thrombophilias
• OCP Use
• Pregnancy
• Malignancy
• Sinusitis 

Evaluation:

• CBC with coagulation profile
• D Dimer (not reliable)
• MRV or CTV(empty delta sign)
• Plain CT (Delta sign, Hemorrhagic infarct  grey white matter junction, hyperdense cervical vein or dural sinus)
• LP may show increased opening pressure

Management:

-Despite risk of hemorrhagic transformation treatment with LMWH or unfractionated heparin shown to reduce Death and dependency.

5. IIH:

Same spectrum of CVT with LP showing increased opening pressure with papilledema and usually young patients, more in females on OCP, but management differs in use of diuretics instead of anticoagulation

6. Carbon monomoxide poisoning:

Multiple patients
Wood burning stove gathering

CT may show bilateral hypodensities

7. Glaucoma: Photophobia, Eye exam mandatory

8: Temporal Arteritis: Other systemic sign and symptoms of disease, PMR, jaw claudication, Blurring of vision, retinal ischemia, check ESR)

9.
Hypertensive encephalopathy ( Altered LOC, Papilledema)

Others::

• Meningitis, encephalitis
• Tumor
• Pre-eclampsia
• Drugs
• Toxins
• Substance abuse, etc

Disclaimer: This don't replace guidelines, follow local protocols.