Syncope [causes, Ddx]; Obliterative Arterial disease of the lower limbs [treatment forms: conservative, interventional and surgival]

Question 1

What is Syncope?

Answer 1

It is the transient loss of consciousness with rapid and spontaneous recovery. It is secondary to Cerebral hypoperfusion having Cardiac causes and Non-cardiac causes.

It usually is preceeded by a Pre-Syncope stage where a patient may feel Lightheardedness, Dizziness, Visual alterations, Change in mental status without loss of consciousness. Pre-Syncope may or may not be followed by Syncope

Question 2

Cardiac and Non-cardiac causes

Various Etiologies for Syncope

Answer 2

Cardiac Syncope:
Arrhythmogenic Syncope: Bradyarrhythmias and Tachyarrhythmias that decreased EF
- Sick Sinus Syndrome
- Ventricular Tachycardia
- AV blocks [especially Mobitz Type II and 3rd degree]
- Supraventricular arrhythmias
- Torsades de Pointes

Cardiovascular Syncope: Myocardial dysfunction or Cardiac outflow obstruction
- Massive MI
- Aortic Stenosis
- Mitral valve prolapse
- ASCVD
- PE
- PH
- HCM
- Cardiac tamponade
- Severe asymmetric septal hypertrophy [aka HOCM]

Non-cardiac Syncope:
Reflex Syncopes: Vasovagal response aka Excessive Vagal tone OR Carotid Sinus sensitivity
- Vasovagal Syncope/Neurocardiogenic Syncope [Prolonged standing, Emotional stress, Pain or Injury]
- Situational Syncope [Cough, Swallow, Laughing, Micturition]
- Carotid Sinus Syndrome [due to Carotid Sinus sensitivity where there is excessive loss of BP from carotid sinus stimulation]

Orthostatic Syncope: Orthostatic Hypotension and Postural Tachycardia Syndrome [POTS]
- Hypovolemia [Diuretic use, dehydration, hemorrhage]
- Beta blockers, CCBs, Alpha blockers and other drugs that cause vasodilation or limit tachycardia
- Prolonged bed rest
- Anemia
- Age related baroreceptor sensitivity loss
- Diabetic neuropathy, Parkinsons Disease [Neurogenic Orthostatic hypotension]
- POTS [poorly understood, often following medical conditions like surgery, trauma, viral illness, pregnancy]

Cardiac Syncopes tend to be much more life threatening, thus immediate management and diagnosis is key to prevent Syncope related mortalities

Question 3

Differential Diagnosis for Syncope aka Transient loss of consciousness

Answer 3

Seizures:
Clinical features:
- Prodrome possibly of an aura [visual, motor, somatosentory, vestibula, vocal or olfactory symptoms]
- Ictal phase focal or generalized
- Postictal phase of imparied consciousness, confusion or residual neurologic symptoms
- Difficult to differential between Tonic-clonic seizures and Convulsive Syncope

Dx findings:
- Elevated Lactate
- Brain CT/MRI may show lesions, bleeding or infection
- Abnormal EEG
- Normal Tilt Table Test [Convulsive syncope induces seizures with hypotension and bradycardia]

Psychogenic pseudosyncope

Subclavian Steal Syndrome:
Clinical features:
- Triggered when straining ipsilateral arm
- Stenosis in subclavian artery proximal to Vertebral artery, forcing contralateral vertebral artery to aid in blood supply to affected side
- Focal neuologic signs like double vision, dysarthria during attack

Dx findings:
- Duplex US of Carotid and Subclavian arteries showing stenosis

Hypoglycemia:
Clinical features:
- History of DM and antidiabetic medications
- Low blood sugar
- Anxiety, tremor, sweating
- Relief in symptoms with increase in blood sugar

Trumatic Brain Injury:
Clinical features:
- History of trauma

Dx findings:
- Brain imaging shows edema, cranial fractures and/or bleeding

Heatstroke

Acute Hyperventilation Syndrome:
Clinical features:
- Tachypnea, Dyspnea, Agitation
- Possible parasthesis and tetany
- History of Panic disorders

Dx findings:
- ABG showing respiratory alkalosis

Drop Attacks:
- Sudden collapse without loss of consciousness
- Possibly due to Vertibrobassilar insufficiency, TIA, Stroke, Seizure, Vestibular dysfunction
- In older patients called Cryptogenic Drop attacks as possible etiology difficult to conclude

Question 4

ASCVD, Claudication, infections need to be treated

PAD Treatment strategies

Answer 4

ASCVD risk management:
- Lifestyle modifications [smoking cessation and recommendation for Quiting programs]
- Lipid Lowering therapy for ASCVD [High intensity Statins | High risk patients Ezetimibe +/- PCSK9 inhibitors]
- Antiplatelet therapy [Aspirin/Clopidogrel]
- HTN management [BP target < 140 mmHg SBP and < 90 mmHg DBP]
- Diabetes management [Metformin | HbA1c goal < 7%]

Structured Exercise Therapy:
- Help patients with Claudication regain some functional capacity of movement without pain
- Helps improve collateral blood supply, however benefits are modest
- First line for claudication management
- Consider before revascularization
- It DOES NOT improve Ankle-Brachial Index

Vasodilators:
- For candidates not suitable for revascularization and patients not benefitting from Structured exercise therapy or risk factor modifications
- Cilostazol [PDE3 inhibitor] is first line agent with vasodilatory, antiplatelet and antithrombotic activity
- Contraindicated in CHF patients
- Improvement signs take upto 12 weeks. If no noticable improvement in symptoms, discontinue

Revascularization:
- For Critical Limb Ischemia patients and Life-limiting claudication patients not improving from other therapies
- Endovascular or Surgical Revascularization

Supportive Care:
- Foot care [teach patients on proper foot care; Urge them to report new infections in diagnosed PAD cases to doctors]
- Analgesia
- Wound management

Amputation:
- Reserved for PAD cases causing Wet or Dry Gangrene
- Wet Gangrene - unsalvagable limb, especially with sepsis need urgent amputation
- Dry Gangrene - evaluate revascularization before amputation