RMedistive

🟣 Evaluation:-
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HAPE's clinical diagnosis would include at least two of the following symptoms or complaints: chest tightness or pain, cough, dyspnea at rest and decreased exercise tolerance.

It also would have two of the following exam findings: central cyanosis, rales/ wheezes , tachycardia and tachypnea.

If available, CXR may show patchy alveolar infiltrates with normal- sized mediastinum/ heart and ultrasound may show B- lines consistent with pulmonary edema.

ECG may show signs of right axis deviation and/or ischemia.

In a patient with infiltrates on CXR, rapid correction of clinical status and SpO2 with supplemental oxygen is pathognomonic of HAPE.

...... treatment next..!

🟣 Differential diagnosis:-
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👉🏻 Asthma

👉🏻 Bronchitis

👉🏻 Mucous plugging

👉🏻 Myocardial infarction

👉🏻 Pneumonia

👉🏻 Pneumothorax

👉🏻 Pulmonary embolism

👉🏻 Upper respiratory tract infection

....to be continued

🟣 History and physical:-
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HAPE typically occurs 2 to 5 days after arrival at altitude.

It has an insidious onset with a non- productive cough, decreased exercise tolerance , chest pain, and exertional dyspnea.

Without treatment, it can progress to dyspnea at rest and severe exertional dyspnea.

A cough may become productive of pink and frothy sputum or frank blood.

The patient may also have rales or wheezes, central cyanosis , tachypnea and tachycardia .
SpO2 is often 10% less than expected for altitude, and the patient often will appear better than expected given their level of hypoxemia and SpO2 value, which typically resides around 40% to 70%.

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This allows for a more adequate delivery of oxygen to the tissues, particularly muscle tissues that may be under greater levels of stress due to exertion with climbing and / or trekking.
If the HVR is blunted, due to genetic predisposition or sedatives , it will lead to further hypoxia causing a non- uniform, exaggerated hypoxemic pulmonary vasoconstriction (HPV).
This pulmonary vasoconstriction then results in increased perfusion to affected alveoli, causing increased hydrostatic stress/ pressure and thus increased mechanical stress on the blood- gas barrier.
Damage to the blood gas barrier results in increased capillary permeability and subsequent non- uniform pulmonary edema.
This edema formation impedes oxygen transport, resulting in more widespread and worsening HPV.
Sympathetic stimulation and circulating vasoconstrictors from the HPV response result in vasoconstriction , worsening pulmonary hypertension , and increasing capillary pressures.
If an individual lacks innate adaptation to these organ level changes or the condition is not recognized or treated , the disease condition will persist and continue to worsen.

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There are four potential adaptations to overcome the constraints of high altitude hypoxia : 1) resting ventilation 2) hypoxic ventilatory response 3) oxygen saturation of arterial hemoglobin and 4) hemoglobin concentration.

Studies of population in the Andes and Tibetian ranges and ranges have shown different adaptive changes between groups despite being at the same altitude.
Those from Tibet had mean 0.5 standard deviations above that of the Aymara people of the Andes for the first two traits and a full standard deviation below for the latter two traits.

The research suggests a genetic predisposition to how different groups of people at the same altitude may adapt to high altitude stress.
For those traveling to a high altitude for a short period, minute ventilation tends to be the mechanism by which trekkers from low altitude will acclimate.

In general, it takes as much as 1 to 2 weeks for the erythropoietin levels to increase enough to cause hematopoiesis and increased circulating hemoglobin.

As one enters higher elevations, minute ventilation increases almost immediately and respiratory alkalosis ensues.

This causes a shift in the oxygen disassociation curve to the left ( increased affinity of oxygen by hemoglobin.)

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🟣 Pathophysiology:-
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The development of HAPE occurs as a response of the pulmonary vasculature to hypoxia.
At altitude, the body responds to hypoxia by hyperventilation.
This is known as the hypoxic ventilatory response ( HVR ).
This response varies between individuals and has a genetic component.
High altitude adaptation is an interesting phenomenon that regularly applies to individuals living at altitude for longer periods of time but is not usual for those visiting altitude.
Understanding the principles of tissue oxygen delivery , however, is useful when considering the effects and adaptations of those coming from higher barometric pressures to the lower pressures of high elevation.

The concentration of oxygen in 1 liter of air at sea level is 21%.
This concentration is the same at 4000meters (~13,200 feet), but due to decrease barometric pressure at this altitude, only 63% of the number of available oxygen molecules remain as compared to sea level.
Thus , to adequately deliver oxygen to the tissues , particularly those that are the most in need of the oxygen for aerobic metabolism ( brain, heart, lungs , kidneys ), certain adaptations must occur.

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🟣 Epidemiology:-
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The severity of HAPE will depend on multiple factors including altitude, initial recognition and management, and access to medical care.

At 4500 meters the incidence is 0.6% to 6 % and at 5500 meters the incidence is 2%to 15% , with the fastest ascent time correlating to a higher incidence.

Those with prior incidence of HAPE have a recurrence rate as high as 60%.

One's level of fitness is not proven to be a protective factor.
Mortality rate, when treated , can be as high as 11% and as high as 50% when untreated.

UpTo 50% of cases may have concomitant acute mountain sickness ( AMS )and Up to 14% will have concomitant high altitude cerebral edema ( HACE ).

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⭐HIGH ALTITUDE PULMONARY EDEMA:-
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High Altitude Pulmonary Edema ( HAPE ) is a severe form of high altitude illness that, if left untreated, can lead to mortality in 50 percent of affected individuals.

It occurs secondary to hypoxia, and is a form of noncardiogenic pulmonary edema.

It is characterized by fatigue, dyspnea, and a dry cough with exertion.

If left untreated, it can progress to dyspnea at rest, rales and cyanosis.

🟣Etiology:-
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Along with other illnesses related to altitude, HAPE occurs above 2500 meters but can occur at altitudes as low as 2000 meters.

Risk factors include individual susceptibility due to low hypoxic ventilatory response (HVR), the altitude attained , a rapid rate of ascent, male s*x, use of sleep medication , excessive salt ingestion, ambient cold temperature and heavy physical exertion.

Preexisting conditions such as those leading to increased pulmonary blood flow , pulmonary hypertension, increased pulmonary vascular reactivity or patent foramen ovale may have a higher disposition towards the development of HAPE.

Today we are going to discuss
HAPE ........High Altitude Pulmonary Edema....

Scenario:- A 20 year old male patient presented to the hospital, weight 98kg, with active complaints of shortness of breath, cough on exertion and fatigue. Vitals:- Pulse rate= 88bpm, B.P= 180/100mmhg , Spo2 = 91 %
Temp=99°F. He also had an oliguria.

This patient had a history of tours to northern areas, not much of a height but developed sudden shortness of breath, after which he was shifted to near by hospital and then to hospital in Sialkot.

HAPE :- High Altitude Pulmonary Edema...

Happy 77th Independence Day ......
Pakistan Zindabad...🫶🏻🫶🏻🇵🇰🇵🇰💖💖

💉💉 Types of injections:-
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🔸 Intramuscular:- Angle=90°

🔸 Subcutaneous:- Angle=45°

🔸 Intravenous:- Angle= 25°

🔸 Intradermal:- Angle= 10°- 15°

⚾ Prognosis:-

Patients with Gilbert Syndrome have an excellent prognosis.

Outcomes of patients with Gilbert syndrome are similar to that of the general population.

The possible beneficial effects of mild unconjugated hyperbilirubinemia include a lower incidence of atherosclerosis, endometrial cancer, Hodgkin's lymphoma and cancer related mortality.

⚾ Complications:-

Gilbert syndrome is a benign, autosomal recessive inherited disorder of bilirubin metabolism.

Consequently, patients with this condition are not at significant risk of progressive liver disease, hepatic decompensation , or liver related mortality.
Patients and their families should be informed of the inherited and benign nature of disease , and unnecessary testing should be kept to the minimum.

As mentioned above, if there is any clinical suspicion of acute or chronic liver disease based upon the clinical presentation or laboratory studies, a more thorough evaluation should be undertaken for viral, metabolic and autoimmune liver diseases.

The End 📚📑🧾📖🎒😷👩🏻‍⚕️🏥🥼🩺💊🩻🚑⚖️