We present an unusual case of hypoxemia that was difficult to diagnose. The clinical scenario contained several small clues which when added up could perhaps, in retrospect at least, have led to timely diagnosis if they had been identified earlier. As this is a condition often discrete yet important for the physician to recognize we have presented the case for others to learn from. It contains interesting learning points on how to approach the hypoxic patient. We have used the opportunity to review basic lung physiology relevant to the clinician.

A 75 year old female, smoker, presented to the emergency department in an ambulance after being found on the floor of her apartment. She was fully conscious but had left-side hemiparesis and dysarthria. She was dyspneic and complained about bilateral pain low in the chest, radiating to the back.

Previous history was of hypertension and “some kind of arrhythmia” and she was currently taking antihypertensive tablets, ASA and zopiclone. There was no history of lung disease.

Examination and labs

BP 162/102, pulse 112/min
temp 37°C
RR 28/min, sat 84% with 6L O2 on a simple face-mask

Cardiac auscultation: normal
Pulmonary auscultation: prolonged expiration, bronchial sounds with fine crackles at the base.
Chest: A fresh bruise at approximately 6-7th rib on the left side, laterally to midclavicular line.
Neurological examination: dysarthria, flaccid hemiparesis of left side.
Labs:

WBC 8.6, CRP 29
Hemoglobin 170, platelets 115
Na 142 K 3.6 creatinine 73
D-dimer 8.47 (<0.25), CK 2.933

ECG: atrial fibrillation 108/min, otherwise normal
CT head: Old infarcts at basal ganglia bilaterally, old infarct in left temporal lobe. No fresh infarcts, no intracranial bleeding.

tPA was judged as not appropriate as time from onset of stroke was far too long. Admission to neurology was prepared but patient was stuck in ED as there were no beds available in hospital.

It was noted that she was persistently hypoxic and not responding to O2 despite general maneuvers (increased FiO2, sitting patient up).

Why is the patient be better oxygenated by sitting up?

V/Q and shunting physiology is complicated but it is quite clear that body position affects both ventilation and perfusion (eg. use of prone position for patients with ARDS in ICU). All in all, supine position tends to decrease patient's own breathing and collapse alveoli in posterior (dependent) part of the lung - this leads to increased 'physiological (right to left) shunting' which is otherwise discrete and nonsignificant in the healthy subject. Patient sitting up or with head elevated (20-30') will do more efficient breathing (ventilation) and open more alveoli and decrease V/Q mismatch.
[Phys. Ther. 1985] Effect of Body Position on Pulmonary Function

An ABG was drawn (with 10L of O2):

pH = 7.46
pO2 = 52mmHg (80-100)
pCO2 = 31mmHg (34-46)
HCO3 = 24 (22-26)
(calculated) SaO2 = 87%

How do you interpret the ABG?

Uncompensated, mild respiratory alkalosis and hypoxia. Patient is hyperventilating to compensate for hypoxic state. Notice that pCO2 is not elevated, an important clue in the underlying condition.

Does the patient need to be intubated?

This patient does not have an immediate need of endotracheal intubation but certainly has a risk of decompensating fast due to exhaustion from hyperventilating, further decreasing SaO2 and starting a downward spiral of rising pCO2 and acidosis. We should keep in mind that having a SaO2 of 86%, this patient is at the rim of the steep slope of the oxygen–haemoglobin dissociation curve and there is no room for further desaturation.

Hypoxia management - ABC first!

Endotracheal ntubation is not risk free and there are still other options to help this patient. Emergency physicians are trained to always have a plan B and C, being mentally prepared for intubation is wise in this scenario and the patient should absolutely be placed in the critical care bay where the airway wagon is near.

A - Airway: patient is awake and protects her airway, excluding need of nasopharyngeal (Guedel) airway
B - Breathing: patient breathes spontaneously and does not need BVM assisted ventilation. FiO2 is 100% but flow can be increased so we change from simple mask to 15L O2 on reservoir mask which theoretically can supply lungs with approximately 80% oxygen.
C - Circulation: is not a problem here, she has minor tachycardia but not so that it reduces carriage of O2 to tissues.

This is a good time to review possible routes of oxygenation, although FiO2 from wall is 100% it can be difficult to provide the patient with air 100% saturated with O2 molecules.Oxygen therapy devices

Plan B - high flow O2 in nasal cannula!

Using the nasopharyngeal route for oxygenation has until recently been thought to provide only limited O2 to the lungs but airway guru Richard Levitan has proven otherwise and his work has led to game changers in approaching the desaturated patient. These two articles introduced the main publication in layman language; [EpMonthly] The neglected orifice [EpMonthly] No desat!

In our case we’d throw on 15L of 100% FiO2 with a nasal cannula and ensure patient is sitting upright - this simple maneuver would most likely be enough to prevent an unnecessary RSI. BIPAP is not recommended if patient is tired or drowsy but a CPAP trial could easily be done.

The articles mentioned above have been widely accepted by front-line emergency physicians as breakthrough publications for airway management and considered a must-read for every physician practising airway management especially RSI. The authors, Richard Levitan and Scott Weingart, are both highly respected teachers of airway and high-intensive care management and one of todays most wanted speakers in emergency medicine conferences. Luckily they are also advocators of FOAM and thus provide most of their material on the world wide web, free of charge!

Hypoxia workup

We now had time to focus on the cause of hypoxia. The patient had no fever thus pneumonia was considered unlikely. With the bruised left chest wall, pneumothorax was considered and bedside ultrasound done. The ultrasound found absence of lung sliding (not normal!) on left side so a chest x-ray was ordered to evaluate for suspected pneumothorax. Noticeably, there were no signs of pleural fluid and absence of B-lines, ruling out hemothorax and pulmonary edema.

What is the DDX for lack of lung sliding on ultrasound

pneumothorax
pleural effusion
massive consolidation/atelactasis
pulmonary contusion
advanced COPD
pleural adhesion/pleurodesis
severe fibrosis
if intubated

mainstem intubation
poor ventilation

[Sonosite] Lung sliding explained

Bedside CXR showed no signs of pneumothorax but elevated left diaphragm and mediastinal shift to left side, indicating decreased left lung volume.

Formal radiologist review: “Decreased volume of left lung with shift of mediastinum and trachea to the left side. No evident infiltrates but suspected smaller peribronchial consolidations behind cardiac contour. No pulmonary stasis. “

Pneumonia could not be excluded even with lack of fever (remember elderly patients commonly have inappropriate vital signs) but ARDS was ruled out.

The meaning of mediastinal shift was not clear at this moment and the grossly elevated D-dimer value could not be explained so the next logical step was to have order a CT angiography of the lungs. Avid readers should by now be able to make a definite diagnosis as enough clues have stacked up!

What is the DDX for mediastinal shift?

1. Pulled (loss of lung volume)

atelectasis
fibrosis
agenesis
surgical resection
pleural fibrosis

2. Pushed (space occupying lesions)

pleural effusion
pneumothorax
large mass lesions

3. Mediastinal masses and thyroid tumors
4. Kypho-scoliosis

Radiologist's answer: "No sign of pulmonary embolism. Small consolidations posterobasally left side. No pathological lymph nodes. No pneumothorax."

Progress

IV antibiotics were initiated and we decided to consult the pulmonologist who then asked the radiologist to review the CT which on more thorough examination revealed a bronchial mucous plug (marked by red arrow at 0:28 in video). The patient went for bronchoscopy where the plug was drawn out and SaO2 rose.

Final diagnosis: obstruction atelectasis secondary to mucous plug. Not surprising for a patient - a smoker - who has been lying immobilised for a longer time with pain in thorax, restricting air movement and dehydration contributing to the mucus buildup. Not unlikely she also has an undiagnosed, underlying COPD.

Finally - why was the D-dimer increased in this patient?

D-dimer is probably the single most incorrectly used lab test in the ED, commonly leading to unnecessary CTs. Remember, d-dimer was designed to RULE-OUT thrombosis in low-risk settings - the way we're using it today is no how it was supposed to be!
A study made 2007 demonstrated that immobility can elevate D-dimer titers by 50-60%. Other conditions and habits of the patient are also known to elevate D-dimer titres. Of the non-pathologic reasons include cigarette smoking and old age and pathological conditions including atrial fibrillation, stroke and infection. [LITFL] Dealing with d-dimer debacles

Atelectasis

Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology and leads to a deflated lung segment or even whole lung collapse causing hypoxia. There are several different types of atelectasis, depending on the cause, as exlained below.

The video above shows how recruitment (=PEEP + ventilation) re-expands a deflated lung and helps us understand the importance of atelectasis. Lung collapse is atelectasis of the whole lung.

Atelectasis is primarily obstructive or non-obstructive, seperated mainly by their pathophysiology. Common causes of obstruction are foreign bodies, tumors and mucus plugs and the size of atelectasis mostly depends on where the obstruction is located (main-, lobal- or segmental bronchi). Obstructive atelectasis (the more common type) is also called resorptive atelectasis, refering to gas absorption distal to the obstruction. In a few hours this leads to retraction of the affected lung and ventilation-perfusion (V/Q) mismatch and shunting as circulating blood is not oxygenated. Secondary infection may occur. If the area is large there will be significant volume loss of the affected lung and secondary hyperinflation of the healthy lung leading to the distinct x-ray features of elevated diaphragm and mediastinal shift towards affected area.

Chronic atelectasis will eventually lead to fibrosis and widening of the bronchi, better known as bronchiectasis.

Non-obstructive atelectasis is caused by loss of contact between parietal- and visceral pleura and shares the same final outcome or total lung collapse. There are different types of non-obstructive atelectasis as well. Relaxation/passive atelectasis is caused by pneumothorax or pleural effusion, compression atelectasis caused by any-space occupying lesion within the chest and adhesive atelectasis by any disruption in surfactant, classically ARDS.

Atelectasis has many faces and the key to understanding its presentation, diagnosis and treatment is to know basic lung anatomy and the pathophysiologic mechanism. A detailed description of these can be found in the following excellent articles from eMedicine;Atelectasis Pulmonary Atelectasis (pediatrics)

Atelectasis is a common concern in the ICU and post-operative ward. Decreased respiratory movements (eg. pain, diaphragma irritation), dehydration, O2 therapy and prolonged bed rest all contribute to atelectasis. The main methods to "recruit" alveoli are active adjustment of ventilator PEEP settings and the work of respiratory therapists encouraging patients to sit up and breathe properly with PEEP valves.

Symptoms and signs

They symptoms of atelectasis are subtle and non-specific; hacking, dry cough and sometimes mild fever. As atelectasis grows larger symptoms of hypoxia will dominate - cyanosis, dyspnea, tachycardia etc. On physical examination, dimishing breathing sounds may be the only clue.

Radiology

Plain chest X-ray (PA) is usually enough to diagnose the presence of an atelectasis but does neither define the type nor the exact cause.

Direct signs:
- displacement of interlobar fissueres (most reliable)
- crowding of broncho-vascular markings
- increased lung opacity (non specific)
Indirect signs:
- hilar displacement
- mediastinal shift
- diaphragmatic elevation
- Compensatory hyperinflation (if chronic)

In case of obstruction atelectasis air bronchograms are typically not present unlike the non obstructive types. The exact CXR signs to look for differ depending on which segment is involved. The signs are somewhat complicated, however, this short illustrated video gives an excellent explanation

A bedside chest X-ray (AP), as in our case has lower accuracy and will only reveal gross atelectasis and volume reduction of affected side. If there is a concurrent pleural effusion or large mass it can be difficult to define the cause of the atelectasis on CXR alone and CT is needed. CT scan will show the exact size, shape and location of the atelectasis. It can help in differentiating the obstructive type from the non-obstructive type, and serves as a guide for subsequent bronchoscopy. Although the obstructing lesion can be seen it may be difficult to define the exact cause, e.g. whether it is due to a tumor or a mucous plug. Such distinction will often require bronchoscopy and sampling of bronchial material by suction, endobronchial biopsy or transbronchial biopsy.[Radiopedia] Lung atelectasis

Systematic approach to hypoxia

The patient´s data included the following important clues in the systematic approach to hypoxia:

pCO2 was not increased and hypoxia therefore not caused by hypoventilation
A-a gradient was very high or 622mmHg (expected 21.5) excluding the cause to be low inspired O2 (see http://www.mdcalc.com/a-a-o2-gradient)
pO2 was not correctable by giving O2, suggesting shunt rather than V/Q mismatch and shunt is commonly caused by atelectasis, oedema, pneumonia or vascular shunt

Now wait a minute - what is the difference then between shunt and vascular shunt? Why doesn't pO2 increase with O2 when there's a shunt? It's time for a pulmonologist to explain some basic physiology! TIP: use Youtube's play faster feature for 1-2x playback speed (lower right corner)

Pulmonologist's comment

Great case with many aspects and learning opportunities! In brief, if I had seen the patient I would have been immediately worried about the severe hypoxemia with respiratory alkalosis, commonly seen in pulmonary embolism. Therefore a lung CT angiogram would probably have been my first radiology test (I certainly hope so, but these things are so much easier in retrospect), after seeing the blood gas result. No CXR needed and I agree, definitely NO D-dimer! But the CT is difficult to read.
The case reminds us how easy it is to miss the unexpected on imaging studies, and that we should remember to thank our good colleagues in that field on a daily basis.
To view another aspect, this is a smoker with a mediastinal shift on CXR. This combination should make us think about lung cancer with endobronchial involvement. This was appropriately ruled out by bronchoscopy. Mucus plugs are common, especially in chronically ventilated patients, in those with asthma and in those with hypoventilation in general. Conservative treatment with mucolytics and respiratory therapy is often sufficient, however bronchoscopic suction with the help of saline may be required to remove plugs. In severe cases, mostly encountered in the ICU, different types of bronchoscopic instruments may be needed to pull out large, dry, and amazingly hard plugs, such as the one depicted above. Large or small, it is important to follow up on the removal of plugs with mucolytics, bronchodilators and physical therapy for several days to prevent the common problem of recurrence. /Ólafur Baldursson

Summary

So it turns out that the patient had a mucus plug leading to a large atelectasis resulting in hypoxia. The underlying mechanism is shunting where a large obstruction hinders blood flow from pulmonary arteries and redirects it to other areas already well oxygenated. Thus no increase in SaO2 is seen despite high flow FiO2 on a rebreather mask. As described, normal pCO2 is also typical for this type of hypoxia as ventilation itself is mostly unaffected.

A chest X ray can be used to diagnose atelectasis but CT and/or bronchoscopy may be required to find the cause
A-a gradient, pCO2 and pO2 response to oxygen are important to find the underlying cause of hypoxia
Elevated D-dimer is specific for thrombosis but there are many other causes that need to be considered as well

Authors: Bergþóra Þorgeirsdóttir / David Thorisson

Oct 1, 2014

Elderly patient with persistent hypoxia