This patient has come in with worsening shortness of breath and coughing up blood. They have a long history of smoking, and the likely diagnosis is superior vena cava obstruction caused by a primary bronchial tumor.

The typical symptoms of superior vena cava obstruction include breathlessness, chest pain, swelling in the neck, face, and arms, dilated veins and telangiectasia on the arms, neck, and chest wall, facial flushing, stridor due to laryngeal edema, and cyanosis.

Given the severity of the symptoms, this man needs to be urgently referred and admitted to the hospital. To provide immediate relief, his head should be elevated and he should be given supplemental oxygen. Corticosteroids and diuretics may also be administered. Further investigation through CT scanning is necessary, and radiotherapy may be recommended as a treatment option.

Respiratory acidosis occurs when the respiratory system is unable to effectively remove carbon dioxide from the body, leading to an increase in acidity. This is often seen in cases of opioid overdose, where respiratory depression can occur. In respiratory acidosis, the bicarbonate levels may rise as the body’s metabolic system tries to compensate for the increased acidity.

Further Reading:

Arterial blood gases (ABG) are an important diagnostic tool used to assess a patient’s acid-base status and respiratory function. When obtaining an ABG sample, it is crucial to prioritize safety measures to minimize the risk of infection and harm to the patient. This includes performing hand hygiene before and after the procedure, wearing gloves and protective equipment, disinfecting the puncture site with alcohol, using safety needles when available, and properly disposing of equipment in sharps bins and contaminated waste bins.

To reduce the risk of harm to the patient, it is important to test for collateral circulation using the modified Allen test for radial artery puncture. Additionally, it is essential to inquire about any occlusive vascular conditions or anticoagulation therapy that may affect the procedure. The puncture site should be checked for signs of infection, injury, or previous surgery. After the test, pressure should be applied to the puncture site or the patient should be advised to apply pressure for at least 5 minutes to prevent bleeding.

Interpreting ABG results requires a systematic approach. The core set of results obtained from a blood gas analyser includes the partial pressures of oxygen and carbon dioxide, pH, bicarbonate concentration, and base excess. These values are used to assess the patient’s acid-base status.

The pH value indicates whether the patient is in acidosis, alkalosis, or within the normal range. A pH less than 7.35 indicates acidosis, while a pH greater than 7.45 indicates alkalosis.

The respiratory system is assessed by looking at the partial pressure of carbon dioxide (pCO2). An elevated pCO2 contributes to acidosis, while a low pCO2 contributes to alkalosis.

The metabolic aspect is assessed by looking at the bicarbonate (HCO3-) level and the base excess. A high bicarbonate concentration and base excess indicate alkalosis, while a low bicarbonate concentration and base excess indicate acidosis.

Analyzing the pCO2 and base excess values can help determine the primary disturbance and whether compensation is occurring. For example, a respiratory acidosis (elevated pCO2) may be accompanied by metabolic alkalosis (elevated base excess) as a compensatory response.

The anion gap is another important parameter that can help determine the cause of acidosis. It is calculated by subtracting the sum of chloride and bicarbonate from the sum of sodium and potassium.

In this case, the most appropriate target parameter to guide oxygen therapy would be an SpO2 (oxygen saturation) level of greater than 94%.

Further Reading:

There are multiple definitions of sepsis, leading to confusion among healthcare professionals. The Sepsis 3 definition describes sepsis as life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis 2 definition includes infection plus two or more SIRS criteria. The NICE definition states that sepsis is a clinical syndrome triggered by the presence of infection in the blood, activating the body’s immune and coagulation systems. The Sepsis Trust defines sepsis as a dysregulated host response to infection mediated by the immune system, resulting in organ dysfunction, shock, and potentially death.

The confusion surrounding sepsis terminology is further compounded by the different versions of sepsis definitions, known as Sepsis 1, Sepsis 2, and Sepsis 3. The UK organizations RCEM and NICE have not fully adopted the changes introduced in Sepsis 3, causing additional confusion. While Sepsis 3 introduces the use of SOFA scores and abandons SIRS criteria, NICE and the Sepsis Trust have rejected the use of SOFA scores and continue to rely on SIRS criteria. This discrepancy creates challenges for emergency department doctors in both exams and daily clinical practice.

To provide some clarity, RCEM now recommends referring to national standards organizations such as NICE, SIGN, BTS, or others relevant to the area. The Sepsis Trust, in collaboration with RCEM and NICE, has published a toolkit that serves as a definitive reference point for sepsis management based on the sepsis 3 update.

There is a consensus internationally that the terms SIRS and severe sepsis are outdated and should be abandoned. Instead, the terms sepsis and septic shock should be used. NICE defines septic shock as a life-threatening condition characterized by low blood pressure despite adequate fluid replacement and organ dysfunction or failure. Sepsis 3 defines septic shock as persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more, along with a serum lactate level greater than 2 mmol/l despite adequate volume resuscitation.

NICE encourages clinicians to adopt an approach of considering sepsis in all patients, rather than relying solely on strict definitions. Early warning or flag systems can help identify patients with possible sepsis.

Whooping cough, also known as pertussis, is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. This highly contagious disease can be passed on to around 90% of close household contacts.

To prevent the spread of whooping cough, Public Health England advises that children with the illness should stay away from school, nursery, or childminders for 48 hours after starting antibiotic treatment. If no antibiotic treatment is given, they should be kept away for 21 days from the onset of the illness. It’s important to note that even after treatment, non-infectious coughing may persist for several weeks.

For more information on how to control infections in schools and other childcare settings, you can refer to the guidance provided by Public Health England.

The BTS guidelines for acute asthma in children recommend administering oral steroids early in the treatment of asthma attacks. It is advised to give a dose of 20 mg prednisolone for children aged 2–5 years and a dose of 30–40 mg for children over 5 years old. If a child is already taking maintenance steroid tablets, they should receive 2 mg/kg prednisolone, up to a maximum dose of 60 mg. If a child vomits after taking the medication, the dose of prednisolone should be repeated. In cases where a child is unable to keep down orally ingested medication, intravenous steroids should be considered. Typically, treatment for up to three days is sufficient, but the duration of the course should be adjusted based on the time needed for recovery. Tapering off the medication is not necessary unless the steroid course exceeds 14 days. For more information, refer to the BTS/SIGN Guideline on the Management of Asthma.

The BTS guidelines categorize acute asthma into four classifications: moderate, acute severe, life-threatening, and near-fatal.

Moderate asthma is characterized by increasing symptoms and a peak expiratory flow rate (PEFR) between 50-75% of the best or predicted value. There are no signs of acute severe asthma present in this classification.

Acute severe asthma is identified by any one of the following criteria: a PEFR between 33-50% of the best or predicted value, a respiratory rate exceeding 25 breaths per minute, a heart rate over 110 beats per minute, or the inability to complete sentences in one breath.

Life-threatening asthma is determined by any one of the following indicators: a PEFR below 33% of the best or predicted value, a blood oxygen saturation level (SpO2) below 92%, a partial pressure of oxygen (PaO2) below 8 kilopascals (kPa), a normal partial pressure of carbon dioxide (PaCO2) between 4.6-6.0 kPa, a silent chest, cyanosis, poor respiratory effort, arrhythmia, exhaustion, altered conscious level, or hypotension.

Near-fatal asthma is characterized by elevated PaCO2 levels and/or the need for mechanical ventilation with increased inflation pressures.

Lung protective ventilation involves several important elements, with low tidal volumes being a crucial component. Specifically, using tidal volumes of 5-8 ml/kg is recommended to minimize the risk of lung injury. Additionally, it is important to maintain inspiratory pressures, also known as plateau pressure, below 30 cm of water to further protect the lungs. Lastly, permissible hypercapnia, or allowing for higher levels of carbon dioxide in the blood, is another key aspect of lung protective ventilation.

Further Reading:

ARDS is a severe form of lung injury that occurs in patients with a predisposing risk factor. It is characterized by the onset of respiratory symptoms within 7 days of a known clinical insult, bilateral opacities on chest X-ray, and respiratory failure that cannot be fully explained by cardiac failure or fluid overload. Hypoxemia is also present, as indicated by a specific threshold of the PaO2/FiO2 ratio measured with a minimum requirement of positive end-expiratory pressure (PEEP) ≥5 cm H2O. The severity of ARDS is classified based on the PaO2/FiO2 ratio, with mild, moderate, and severe categories.

Lung protective ventilation is a set of measures aimed at reducing lung damage that may occur as a result of mechanical ventilation. Mechanical ventilation can cause lung damage through various mechanisms, including high air pressure exerted on lung tissues (barotrauma), over distending the lung (volutrauma), repeated opening and closing of lung units (atelectrauma), and the release of inflammatory mediators that can induce lung injury (biotrauma). These mechanisms collectively contribute to ventilator-induced lung injury (VILI).

The key components of lung protective ventilation include using low tidal volumes (5-8 ml/kg), maintaining inspiratory pressures (plateau pressure) below 30 cm of water, and allowing for permissible hypercapnia. However, there are some contraindications to lung protective ventilation, such as an unacceptable level of hypercapnia, acidosis, and hypoxemia. These factors need to be carefully considered when implementing lung protective ventilation strategies in patients with ARDS.

Croup, also known as laryngo-tracheo-bronchitis, is typically caused by the parainfluenza virus. Other viruses such as rhinovirus, influenza, and respiratory syncytial viruses can also be responsible. Before the onset of stridor, there is often a mild cold-like illness that lasts for 1-2 days. Symptoms usually reach their peak within 1-3 days, with the cough often being more troublesome at night. A milder cough may persist for another 7-10 days.

A distinctive feature of croup is a barking cough, but it does not indicate the severity of the condition. To reduce airway swelling, dexamethasone and prednisolone are commonly prescribed. If a child is experiencing vomiting, nebulized budesonide can be used as an alternative. However, it is important to note that steroids do not shorten the duration of the illness. In severe cases, nebulized adrenaline can be administered.

Hospitalization for croup is uncommon and typically reserved for children who are experiencing worsening respiratory distress or showing signs of drowsiness or agitation.

Whooping cough, also known as pertussis, is a respiratory infection caused by the bacteria Bordetella pertussis. It is transmitted through respiratory droplets and has an incubation period of about 7-21 days. This disease is highly contagious and can be transmitted to around 90% of close household contacts.

The clinical course of whooping cough can be divided into two stages. The first stage is called the catarrhal stage, which resembles a mild respiratory infection with symptoms like low-grade fever and a runny nose. A cough may be present, but it is usually mild compared to the second stage. The catarrhal stage typically lasts for about a week.

The second stage is known as the paroxysmal stage. During this phase, the cough becomes more severe as the catarrhal symptoms start to subside. The coughing occurs in spasms, often preceded by an inspiratory whoop sound, followed by a series of rapid coughs. Vomiting may occur, and patients may develop subconjunctival hemorrhages and petechiae. Patients generally feel well between coughing spasms, and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over time. The later stages of this phase are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures.

Public Health England (PHE) provides recommendations for testing whooping cough based on the patient’s age, time since onset of illness, and severity of symptoms. For infants under 12 months of age who are hospitalized, PCR testing is recommended. Non-hospitalized infants within two weeks of symptom onset should undergo culture testing of a nasopharyngeal swab or aspirate. Non-hospitalized infants presenting over two weeks after symptom onset should be tested for anti-pertussis toxin IgG antibody levels using serology.

For children over 12 months of age and adults, culture testing of a nasopharyngeal swab or aspirate is recommended within two weeks of symptom onset. Children aged 5 to 16 who have not received the vaccine within the last year and present over two weeks after symptom onset should undergo oral fluid testing for anti-pertussis toxin IgG antibody levels. Children under 5 or adults over

SCUBA divers face the potential danger of developing pulmonary barotrauma, which can lead to conditions like arterial gas embolism (AGE) or pneumothorax. Based on the patient’s diving history and clinical symptoms, it is highly likely that they are experiencing a left-sided pneumothorax caused by barotrauma. To confirm the presence of pneumothorax, a chest X-ray is usually performed, unless the patient shows signs of tension pneumothorax. In such cases, immediate decompression is necessary, which can be achieved by inserting a chest tube.

Further Reading:

Decompression illness (DCI) is a term that encompasses both decompression sickness (DCS) and arterial gas embolism (AGE). When diving underwater, the increasing pressure causes gases to become more soluble and reduces the size of gas bubbles. As a diver ascends, nitrogen can come out of solution and form gas bubbles, leading to decompression sickness or the bends. Boyle’s and Henry’s gas laws help explain the changes in gases during changing pressure.

Henry’s law states that the amount of gas that dissolves in a liquid is proportional to the partial pressure of the gas. Divers often use atmospheres (ATM) as a measure of pressure, with 1 ATM being the pressure at sea level. Boyle’s law states that the volume of gas is inversely proportional to the pressure. As pressure increases, volume decreases.

Decompression sickness occurs when nitrogen comes out of solution as a diver ascends. The evolved gas can physically damage tissue by stretching or tearing it as bubbles expand, or by provoking an inflammatory response. Joints and spinal nervous tissue are commonly affected. Symptoms of primary damage usually appear immediately or soon after a dive, while secondary damage may present hours or days later.

Arterial gas embolism occurs when nitrogen bubbles escape into the arterial circulation and cause distal ischemia. The consequences depend on where the embolism lodges, ranging from tissue ischemia to stroke if it lodges in the cerebral arterial circulation. Mechanisms for distal embolism include pulmonary barotrauma, right to left shunt, and pulmonary filter overload.

Clinical features of decompression illness vary, but symptoms often appear within six hours of a dive. These can include joint pain, neurological symptoms, chest pain or breathing difficulties, rash, vestibular problems, and constitutional symptoms. Factors that increase the risk of DCI include diving at greater depth, longer duration, multiple dives close together, problems with ascent, closed rebreather circuits, flying shortly after diving, exercise shortly after diving, dehydration, and alcohol use.

Diagnosis of DCI is clinical, and investigations depend on the presentation. All patients should receive high flow oxygen, and a low threshold for ordering a chest X-ray should be maintained. Hydration is important, and IV fluids may be necessary. Definitive treatment is recompression therapy in a hyperbaric oxygen chamber, which should be arranged as soon as possible. Entonox should not be given, as it will increase the pressure effect in air spaces.