• Sudden onset of left-sided chest pain (as in AD's case).

• Shortness of breath.

  
  

• Other possible symptoms:

  • Rapid breathing (tachypnoea)

  • Rapid heartbeat (tachycardia)

  • Anxiety or restlessness

  • Fatigue (due to low oxygen)
    
    

• Larger pneumothorax = more obvious symptoms.
  
  

2. Physical Examination

• Decreased air entry on the left side during auscultation (found in AD).

• Other possible findings:

  • Hyperresonance on percussion

  • Reduced chest expansion (affected side)

  • Decreased vocal fremitus

  • Tracheal deviation (if tension pneumothorax)
    
    

3. Imaging Tests

• Chest X-ray (First-line imaging)

  • Collapsed left lung (seen in AD).

  • Air in pleural space without lung markings.

  • Black (dark) area visible, lung edge may be seen.
    
    

• CT Scan

  • Done if X-ray unclear.

  • More sensitive for small pneumothorax.

  • Not needed in AD’s case.
    
    

• Ultrasound (E-FAST)

  • Rapid bedside detection.

  • Useful in trauma or emergency settings.
    
    

4. Arterial Blood Gas (ABG)

• Measures:

  • Oxygen level (PaO₂)

  • Carbon dioxide level (PaCO₂)

  • Blood pH
    

• Used to assess severity of respiratory compromise.

• Guides oxygen therapy or ventilation needs.
  
  

Special Emergency: Tension Pneumothorax

• Signs:

  • Very low blood pressure (hypotension)

  • Severe shortness of breath

  • Distended neck veins

  • Tracheal deviation (away from affected side)
    
    

• Immediate treatment required (no delay for imaging)

• Lignocaine (1% subcutaneous):

  • Appropriate for local anesthesia before chest tube insertion.

  • Provides effective pain relief at the procedure site.

• Tramadol (50 mg IV stat):

  • Potentially inappropriate for AD (COPD patient).

  • Risks:

    • Respiratory depression (especially when combined with other CNS depressants).

    • May worsen hypercapnia (CO₂ retention) in COPD.

  • Better alternatives:

    • IV Paracetamol (less respiratory risk).

    • Low-dose morphine (if strong analgesia needed, but with caution).

2. Appropriateness of Overall Treatment

• Chest tube insertion: Correct for large pneumothorax.

• Underwater seal drainage: Proper management.

• Supplemental oxygen: Initially correct, but must be monitored (risk of CO₂ retention in COPD).

• No mechanical ventilation: Appropriate since AD was stable post-chest tube insertion.

• Drug-induced (from tramadol + diazepam).

• ABG findings:

  • Respiratory acidosis (↓pH, ↑pCO₂, ↑HCO₃⁻)

  • Hypoxemia (pO₂ 60 mmHg)

• Excessive oxygen worsened CO₂ retention (common in COPD)

2. Antidote & Corrective Management

• Naloxone (for tramadol-induced respiratory depression):

  • Dose: 0.04–0.4 mg IV (titrated to avoid withdrawal)

• Flumazenil (for diazepam overdose, but caution in COPD):

  • Dose: 0.2 mg IV, repeat if needed (risk of seizures)

• Oxygen therapy adjustment:

  • Target SpO₂ 88–92% (to avoid CO₂ narcosis).

• Non-invasive ventilation (BiPAP):

  • Needed if hypercapnia persists.

3. Prevention of Recurrence

• Avoid opioids/benzodiazepines in COPD patients.

• Use safer analgesics (e.g., paracetamol, NSAIDs).

• Smoking cessation counseling (to prevent pneumothorax recurrence)

-          Commonly begin with chest pain

-          Shortness of breath

-          Sharp, stabbing chest that worsens when trying to breath in

-          A larger pneumothorax causes more severe symptoms, including:

-          Bluish color of the skin due to lack of oxygen

-          Rapid breathing and heartbeat

-          Dry, hacking cough

• Pneumothorax causes a fast respiratory rate because the collapsed lung reduces oxygen intake (hypoxia), and the body tries to compensate by breathing faster.
  It also causes a rapid heart rate because the heart pumps faster to deliver the limited oxygen to tissues and maintain blood pressure, especially if major vessels are compressed.
  The stress response (sympathetic activation) further speeds up breathing and heart rate.

• Tramadol → Opioid analgesic

• Diazepam → Benzodiazepine

• Both have central nervous system (CNS) depressant effects.

2. Effect of Tramadol

• Tramadol causes dose-dependent respiratory depression, especially in vulnerable patients like:

  • Those with chronic obstructive pulmonary disease (COPD)

  • Post-pneumothorax patients (like AD)

• Dose-dependent respiratory depression means:

  • Low doses → pain relief

  • High doses → suppression of the brainstem respiratory centers

  • Leads to hypoventilation, CO₂ retention, and at very high doses → respiratory arrest

3. Effect of Diazepam

• Mechanism:

  • Enhances GABAergic transmission

  • Binds to GABA-A receptors at the benzodiazepine binding site

  • Increases the frequency of Cl⁻ channel opening

  • ↑ Cl⁻ influx → Neuron hyperpolarization → ↓ Neuronal firing

  • In brainstem respiratory centers, this leads to suppression of respiratory drive

• Alone, diazepam usually causes mild sedation

• But in patients with:

  • Pre-existing lung conditions (like COPD)

  • Or combined with other depressants (like tramadol)

  • → It can result in dangerous respiratory depression

4. Combined Effect of Tramadol + Diazepam

• The drugs act synergistically to suppress the medullary respiratory centers

• Results in:

  • ↓ Respiratory rate (8–9 breaths/min)

  • Hypoventilation

  • CO₂ retention → pCO₂ = 58 mmHg → Respiratory acidosis

  • ↓ Oxygen saturation (SpO₂ = 88%, pO₂ = 60 mmHg) despite oxygen therapy

↑ HCO₃⁻ (38 mmol/L) → evidence of metabolic compensation for chronic respiratory acidosis

frm an article ->Benzodiazepines are drugs that reduce anxiety and relax the muscles. People use them to treat anxiety and insomnia.

If someone is already taking a benzodiazepine medication such as lorazepam or alprazolam, also taking tramadol can result in sedation, respiratory depression, coma, and even death. https://www.medicalnewstoday.com/articles/325278#drug-interactions

Treating Hypoxemia:
Supplemental oxygen raises blood oxygen levels when the lungs can’t provide enough, often due to conditions like COPD or sleep apnea.

Supporting Organ Function:
Oxygen is vital for energy production. Low levels can harm organs like the brain, heart, and kidneys. Oxygen therapy helps keep them functioning properly.

Improving Quality of Life:
It relieves symptoms like breathlessness and fatigue, improving sleep, energy, and overall well-being.

Pharmacists play a role in long-term management:

• Ensuring proper oxygen therapy at home

• Teaching inhaler and nebulizer use

• Ensuring vaccination (e.g., influenza, pneumococcal) to prevent infections

• Monitoring for drug side effects or addiction to sedatives/opioids

⁃ occurs when air accumulates in the space between the lung and the chest wall (pleural space)

⁃ lead to various symptoms that indicate an imbalance in the chest cavity.

-       SpO₂ is also the saturation of Hb,it is read through a pulse oximeter on the finger using light refraction to estimate the binding of hemoglobin. (desaturated 90% below)

-       If SpO₂ is lower than 92%, this usually suggests the patient will require some amount of supplemental oxygen. Supplemental oxygen can be started and increased to attempt to increase the SpO2 to above 92%. Mechanical ventilation would be a subsequent step when high levels of supplementary oxygen is not adequate to support the patient’s oxygen needs, in order to prevent hypoxic failure.

-       Reasons for mechanical ventilation can fall into three main categories:

o   Hypoxic failure (also called hypoxia) is the inability to oxygenate the body adequately. 

o   Hypercapnia, or high CO₂ levels. If CO₂ increases to a level the body cannot clear by increasing breathing, mechanical ventilation is indicated.

o   Ineffective drive to breathe can occur if there is an injury to the brain or neurological control to breathing.

-       If air is in the pleural space, then the chest tube will be inserted above the second intercostal space at the mid-clavicle line.

-       Importance: Restore negative pressure in pleural space, preventing the lung from collapsing and compressing at the end of exhalation.

-       It is disrupted when air, or fluid and air, enters the pleural space and separates the visceral pleura from the parietal pleura. The lung can't stay expanded, so it collapses partially or fully

Normally, a traditional chest tube drainage system  is connected to a closed chest drainage system will have these three chambers:

1.       Collection chamber

2.       Wet or dry suction control chamber

3.       Water-seal chamber

-       This chamber has a one-way valve that allows air to exit the pleural cavity during exhalation but does not allow it to re-enter during inhalation due to the pressure in the chamber.

-       The water-seal chamber must be filled with sterile water and maintained at the 2 cm mark to ensure proper operation, and should be checked regularly.

-       The water in the water-seal chamber should rise with inhalation and fall with exhalation (this is called tidaling), which demonstrates that the chest tube is patent. Continuous bubbling may indicate an air leak, and newer systems have a measurement system for leaks — the higher the number, the greater the air leak. The water-seal chamber can also monitor intrathoracic pressure 

Surgical Intervention (thoracostomy) : In rare cases where chest tube insertion does not effectively resolve the pneumothorax, surgical intervention may be necessary. The decision for surgery is made by a specialist, such as a thoracic surgeon, who will evaluate the condition and determine the most appropriate course of action.

• Primary spontaneous pneumothorax - This happens in people without known underlying lung disease. It is often attributed to the rupture of small air-filled sacs called blebs, typically located at the top of the lungs. PSP is more common in tall, thin individuals, particularly young men.

• Secondary spontaneous pneumothorax - This occurs in individuals with pre-existing lung conditions that weaken the lung tissue, making it more susceptible to collapse. Common underlying diseases include chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis, tuberculosis, pneumonia, and certain interstitial lung diseases.

2. Traumatic pneumothorax - This type results from an injury to the chest that punctures the lung or chest wall, allowing air to enter the pleural space. Causes can include blunt trauma (e.g. car accidents, falls), penetrating trauma (e.g. stab wounds, gunshot wounds) or rib fractures that lacerate the lung.

3. Iatrogenic Pneumothorax: This is a type of traumatic pneumothorax caused inadvertently by a medical procedure. Examples include lung biopsies, central venous catheter insertion, thoracentesis, and mechanical ventilation (barotrauma).

4. Tension Pneumothorax: This is a particularly dangerous type of pneumothorax where a one-way valve effect occurs. Air enters the pleural space during inhalation but cannot escape during exhalation. This leads to a progressive buildup of pressure, which can collapse the affected lung and shift the mediastinum (the area between the lungs containing the heart, trachea, and major blood vessels) to the opposite side. This shifting can compress the other lung and the heart, leading to severe respiratory distress and cardiovascular collapse. Tension pneumothorax is a medical emergency requiring immediate treatment.

2)Counsel on smoking cessation and provide NRT options if needed

3)Reinforce adherence to COPD medications and follow-up visits

4)Collaborate with other healthcare providers for holistic care (respiratory team, GP, smoking cessation services)

5) Advising on supplemental oxygen to promote pleural air absorption (avoiding high flow in COPD patients)

6) Teach correct inhaler technique

7) Educate on smoking cessation, including offering nicotine replacement therapy (NRT)

8)Explain how to avoid triggers that can worsen COPD or cause pneumothorax recurrence

9) Educate on recognizing signs of respiratory distress or medication side effects

respiratory pharmacists are not just medicine experts but also leaders in sustainability, prevention, and system-wide quality improvement.

• COPD (emphysema, chronic bronchitis)

• Asthma

• Lung cancer

• Pneumonia

• Cystic fibrosis

Severe pneumonia

2. Conditions Affecting Breathing Muscles and Nerves

• Muscular Dystrophy

• Guillain-Barre Syndrome

• Myasthenia Gravis

• ALS

• Parkinson’s Disease

 3. Chest and Back Injuries

Trauma to chest, spine, or brain

4. . Other Medical Conditions

   • Heart problems

   • Severe infections

   • Severe scoliosis

   • Obesity Hypoventilation Syndrome

   • Stroke

     
     

5.  Lifestyle Factors

   • Smoking

   • Alcohol abuse

   • Drug overdose

   • Exposure to smoke/chemicals

   • Severe allergies

6. Other Factors

• Age (older adults = higher risk)

• Family history (respiratory diseases)

• Medical procedures (lung surgery, ventilation)

• Air pollution

• Type: Primary (no underlying lung disease) vs. Secondary (e.g., COPD)

• Size of pneumothorax

• Presence and severity of symptoms

• Risk of recurrence or complications

  
  

Step 1: Determine Type of Pneumothorax

• Spontaneous Pneumothorax is the starting point.

• First, assess if the patient is bilateral or hemodynamically unstable:

  • If YES → Immediate chest drain

  • If NO → Proceed to classify:

Classification:

• Primary: No known lung disease, age usually <50, non-smoker.

• Secondary: Age >50, history of smoking, clinical or radiological signs of lung disease (e.g., COPD).

Step 2: Measure Size and Symptoms

For Primary Pneumothorax:

• If >2 cm rim between lung and chest wall and/or breathless → aspirate

  • Use a 16–18G cannula

  • Remove ≤2.5 L of air

  • If successful (lung re-expands and symptoms improve) → discharge or review

  • If not → chest drain (8–14 Fr)

• If <2 cm and not breathless → observe or discharge with outpatient review in 2–4 weeks

For Secondary Pneumothorax (like AD):

• If >2 cm or breathless → chest drain (8–14 Fr) directly

• If 1–2 cm → aspirate with cannula

  • If successful and lung re-expands (<1 cm rim) → admit for observation

  • If not → insert chest drain

• If <1 cm and no severe symptoms → admit and observe with high-flow oxygen for 24 hours

Applying to AD's case:

AD had:

• Secondary spontaneous pneumothorax due to COPD

• Large pneumothorax on X-ray

• Severe symptoms (dyspnea, chest pain, SpO₂ < 90%)

🟢 Therefore, chest tube with underwater seal was the correct management aligned with BTS guidelines.

Other considerations:

1. High-Flow Oxygen Therapy

• Administered to promote nitrogen washout → helps resorb air from the pleural space faster.
  

• Especially useful in small pneumothorax or post-drainage.
  

Relevance to AD:
He was initially desaturated, so oxygen therapy would have supported his SpO₂ while the lung re-expanded.

2. Needle Aspiration (First-line for PSP)

• A wide-bore needle is inserted into pleural space to remove air (up to 2.5L).
  

• Not typically done in SSP due to high failure rate.
  

Not used in AD:
Because AD had SSP and was severely symptomatic, needle aspiration alone is insufficient.

3. Surgical Options (for recurrent or persistent pneumothorax)

• VATS (Video-assisted thoracoscopic surgery) for:

  • Persistent air leak >5 days

  • Recurrent pneumothorax

  • Failed tube drainage
    

• Pleurodesis: Chemical (talc) or surgical procedure to adhere the lung to chest wall to prevent recurrence.
  

Not yet indicated for AD, unless pneumothorax recurs or persists.

Reference(https://thorax.bmj.com/content/78/11/1143)

Arterial Blood Gas (ABG) is a test that measures the levels of oxygen (O₂), carbon dioxide (CO₂), and acidity (pH) in arterial blood. It helps assess how well the lungs and kidneys are maintaining acid–base balance, and how effectively gas exchange is happening in the lungs.

ABG is a test that measures:

• pH: How acidic or alkaline the blood is.

• PaCO₂: Amount of carbon dioxide (reflects lung function).

• HCO₃⁻ (bicarbonate): Reflects kidney function and compensation.

• PaO₂: Oxygen level in the blood

How It Works (Mechanism):

1. Blood is drawn from an artery (usually radial).

2. A blood gas analyzer measures gas tensions and calculates acid-base balance.

3. Helps differentiate respiratory vs. metabolic disorders and detect respiratory failure.

Using the chart:

1. Identify the Primary Disorder:

• pH = 7.30 → Acidosis

• PaCO₂ = 58 mmHg → ↑ = Respiratory Acidosis

• HCO₃⁻ = 38 mmol/L → ↑ = Renal Compensation

PRIMARY DISORDER: RESPIRATORY ACIDOSIS (↑ CO₂ causes ↓ pH)

+Why Did This Happen to AD?

• AD was given IV diazepam (sedative) and IV tramadol.

• These drugs suppress breathing → slower RR = less CO₂ removed → CO₂ builds up → respiratory acidosis

2. Is Compensation Present?

Look at the bicarbonate (HCO₃⁻) level:

• For chronic respiratory acidosis, every ↑10 mmHg in PaCO₂ → ↑HCO₃⁻ by 4 mmol/L

• Normal PaCO₂ = 40 mmHg → AD’s = 58 mmHg → increase = +18 mmHg

• Expected increase in HCO₃⁻ = 4 × (18/10) = ~7.2 mmol/L

• Normal HCO₃⁻ = 24 → expected ~31.2 mmol/L

• AD’s actual HCO₃⁻ = 38 mmol/L → excessive compensation

🔴 Overcompensated → possible combined metabolic alkalosis or prolonged compensation.

3. Final Diagnosis for AD:

✅ Primary Respiratory Acidosis
➕ Metabolic compensation (HCO₃⁻ retention)
➡ Suggestive of chronic respiratory compromise (likely due to COPD)
➕ Aggravated by CNS depressants (IV diazepam + tramadol) causing hypoventilation
➡ Drug-induced Type 2 Respiratory Failure

Referene: https://www.nursingtimes.net/emergency-and-critical-care/essential-critical-care-skills-6-arterial-blood-gas-analysis-28-03-2022/

https://moh.gov.my/moh/resources/Penerbitan/Program%20Bebas%20Kesakitan/Garis%20Panduan/Pain_Management_in_ETD_2020_(2nd_Ed.)_.pdf

https://www.moh.gov.my/moh/resources/Penerbitan/Hospital%20Bebas%20Kesakitan/Bahan%20Pendidikan/Pain_Management_in_Emergency_Trauma_Department.pdf

https://pmc.ncbi.nlm.nih.gov/articles/PMC4332101/

• Damages lung tissue and slows recovery.

• Increases the risk of another pneumothorax or infection.

• Reduces the effectiveness of inhalers and medications.

Alcohol

• Can suppress breathing, especially if taken with sedatives like tramadol or diazepam.

• Weakens the immune system, increasing infection risk.

• May interact with prescribed medications.

o   This can provide pharmacist to have better judgement and give appropriate medication.

-       Counsel the SE of the medication and the function of medication use(so able to comply)

• Problem: AD has COPD, poor medication adherence, and frequent exacerbations.

• Pharmacist role: Recommends digital tools like medication reminder apps or smart inhalers with Bluetooth tracking (e.g., Propeller Health, Hailie®).

• Impact: Improves inhaler adherence and allows remote monitoring of use patterns by clinicians to pre-empt future exacerbations or pneumothorax risk.

2. 🩺 Transitional Care Coordinator

• Post-discharge, AD is at high risk of readmission.

• Pharmacist coordinates a "meds-to-beds" program, ensuring all discharge meds are ready and the patient understands how and when to take them.

• Conducts a 30-day medication follow-up call to assess adherence, new side effects, and reinforce lifestyle changes.