The guidelines from the European League Against Rheumatism (EULAR) regarding the diagnosis of gout state that if a joint becomes swollen, tender, and red, accompanied by acute pain that intensifies over a period of 6-12 hours, it is highly likely to be a crystal arthropathy. While pseudogout is also a possibility, it is much less probable, with gout being the most likely diagnosis in such cases.

In cases of acute gout, the joint most commonly affected is the first metatarsal-phalangeal joint, accounting for 50-75% of cases. The underlying cause of gout is hyperuricaemia, and the clinical diagnosis can be confirmed by the presence of negatively birefringent crystals in the synovial fluid aspirate.

For the treatment of acute gout attacks, the usual approach involves the use of either NSAIDs or colchicine.

The co-epidemic of tuberculosis and HIV is a significant global health challenge at present. According to the WHO, there were 10 million new cases of tuberculosis in 2019, with approximately 11% of these cases being co-infected with HIV. Tuberculosis is the most common contagious infection in individuals with compromised immune systems due to HIV, often leading to death.

Tuberculosis is caused by an infection with the bacterium Mycobacterium tuberculosis. While it primarily affects the lungs, it can also impact various other parts of the body. The disease is spread through aerosol transmission, meaning it is transmitted through droplets in the air.

The primary symptoms of tuberculosis infection include a chronic cough, coughing up blood (haemoptysis), fever, night sweats, and weight loss. In individuals who have not been previously affected, tuberculosis can cause a primary lesion known as the Ghon focus. This lesion typically develops in the upper lobes of the lungs.

In 15-20% of cases, the infection spreads to extrapulmonary sites such as the pleura, central nervous system, lymphatics, bones, joints, and genitourinary system. Extrapulmonary tuberculosis that affects the spine is known as Pott’s disease, primarily affecting the lower thoracic and upper lumbar vertebrae. Cervical tuberculous lymphadenopathy, also known as scrofula, is characterized by cold abscesses without erythema or warmth.

Only a small percentage of patients, around 5-10%, go on to develop post-primary tuberculosis, also known as reactivation tuberculosis. This typically occurs a year or two after the primary infection and is more likely to happen in individuals with a weakened immune system. Reactivation tuberculosis often involves the lung apex.

The use of antibiotics can impact the effectiveness of warfarin and other coumarin anticoagulants. This can lead to changes in the International Normalized Ratio (INR) and, in severe cases, increase the risk of bleeding. Some antibiotics, such as chloramphenicol, ciprofloxacin, co-trimoxazole, doxycycline, erythromycin, macrolides (e.g., clarithromycin), metronidazole, ofloxacin, and sulphonamide, are known to enhance the anticoagulant effect of warfarin. However, cefalexin is considered relatively safe and is the most suitable option in this situation.

Arterial blood gas (ABG) interpretation is essential for evaluating a patient’s respiratory gas exchange and acid-base balance. The normal values on an ABG may slightly vary between analyzers, but generally, they fall within the following ranges:

pH: 7.35 – 7.45
pO2: 10 – 14 kPa
PCO2: 4.5 – 6 kPa
HCO3-: 22 – 26 mmol/l
Base excess: -2 – 2 mmol/l

In this particular case, the patient’s history indicates an overdose. However, there is no immediate need for intubation as her Glasgow Coma Scale (GCS) score is 11/15, and she can speak, albeit with slurred speech, indicating that she can maintain her own airway.

The relevant ABG findings are as follows:

– Mild hypoxia
– Decreased pH (acidaemia)
– Low PCO2
– Normal bicarbonate
– Elevated lactate

The anion gap is a measure of the concentration of unmeasured anions in the plasma. It is calculated by subtracting the primary measured cations from the primary measured anions in the serum. The reference range for anion gap varies depending on the methodology used, but it is typically between 8 to 16 mmol/L.

In this case, the patient’s anion gap can be calculated using the formula:

Anion gap = [Na+] – [Cl-] – [HCO3-]

Using the given values:

Anion gap = [143] – [99] – [22]
Anion gap = 22

Therefore, it is evident that she has a raised anion gap metabolic acidosis. It is likely a type A lactic acidosis resulting from tissue hypoxia and hypoperfusion. Some potential causes of type A and type B lactic acidosis include:

Type A lactic acidosis:
– Shock (including septic shock)
– Left ventricular failure
– Severe anemia
– Asphyxia
– Cardiac arrest
– Carbon monoxide poisoning
– Respiratory failure
– Severe asthma and COPD
– Regional hypoperfusion

Type B lactic acidosis:
– Renal failure
– Liver failure
– Sepsis (non-hypoxic sepsis)
– Thiamine deficiency
– Al

Legionella pneumophila, a Gram-negative bacterium, can be found in natural water supplies and soil. It is responsible for causing Legionnaires’ disease, a serious illness. Outbreaks of this disease have been associated with poorly maintained air conditioning systems, whirlpool spas, and hot tubs.

The pneumonic form of Legionnaires’ disease presents with specific clinical features. Initially, there may be a mild flu-like prodrome lasting for 1-3 days. A non-productive cough, occurring in approximately 90% of cases, is also common. Pleuritic chest pain, haemoptysis, headache, nausea, vomiting, diarrhoea, and anorexia are other symptoms that may be experienced.

Fortunately, Legionella pneumophila infections can be effectively treated with macrolide antibiotics like erythromycin, or quinolones such as ciprofloxacin. Tetracyclines, including doxycycline, can also be used as a treatment option.

While the majority of Legionnaires’ disease cases are caused by Legionella pneumophila, there are several other species of Legionella that have been identified. One such species is Legionella longbeachae, which is less commonly encountered. It is primarily found in soil and potting compost and has been associated with outbreaks of Pontiac fever, a milder variant of Legionnaires’ disease that does not primarily affect the respiratory system.

Loop diuretics, like furosemide, commonly result in several electrolyte imbalances. These imbalances include hyponatremia, which is a decrease in sodium levels in the blood. Another common imbalance is hypokalemia, which refers to low levels of potassium. Additionally, loop diuretics can cause hypocalcemia, a condition characterized by low levels of calcium in the blood. Another electrolyte affected by loop diuretics is magnesium, as they can lead to hypomagnesemia, which is a deficiency of magnesium. Lastly, loop diuretics can cause hypochloremic alkalosis, which is a condition characterized by low levels of chloride in the blood and an increase in blood pH.

Anaemia of chronic disease is a type of anaemia that can occur in various chronic conditions, such as rheumatoid arthritis, systemic lupus erythematosus, tuberculosis, malignancy, malnutrition, hypothyroidism, hypopituitarism, chronic kidney disease, and chronic liver disease. The underlying mechanisms of this type of anaemia are complex and not fully understood, with multiple contributing factors involved. One important mediator in inflammatory diseases like rheumatoid arthritis is interleukin-6 (IL-6). Increased levels of IL-6 lead to the production of hepcidin, a hormone that regulates iron balance. Hepcidin prevents the release of iron from the reticulo-endothelial system and affects other aspects of iron metabolism.

Anaemia of chronic disease typically presents as a normochromic, normocytic anaemia, although it can also be microcytic. It is characterized by reduced serum iron, reduced transferrin saturation, and reduced total iron-binding capacity (TIBC). However, the serum ferritin levels are usually normal or increased. Distinguishing anaemia of chronic disease from iron-deficiency anaemia can be challenging, but in iron-deficiency anaemia, the TIBC is typically elevated, and serum ferritin is usually low.

The earliest and most common clinical indication of malignant hyperthermia is typically an increase in end tidal CO2 levels.

Further Reading:

Malignant hyperthermia is a rare and life-threatening syndrome that can be triggered by certain medications in individuals who are genetically susceptible. The most common triggers are suxamethonium and inhalational anaesthetic agents. The syndrome is caused by the release of stored calcium ions from skeletal muscle cells, leading to uncontrolled muscle contraction and excessive heat production. This results in symptoms such as high fever, sweating, flushed skin, rapid heartbeat, and muscle rigidity. It can also lead to complications such as acute kidney injury, rhabdomyolysis, and metabolic acidosis. Treatment involves discontinuing the trigger medication, administering dantrolene to inhibit calcium release and promote muscle relaxation, and managing any associated complications such as hyperkalemia and acidosis. Referral to a malignant hyperthermia center for further investigation is also recommended.

Malaria is a contagious illness that is spread by female mosquitoes of the Anopheles genus. It is caused by a parasitic infection from the Plasmodium genus. There are five species of Plasmodium that can cause disease in humans: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, Plasmodium malariae, and Plasmodium knowlesi.

The main symptom of malaria is the malarial paroxysm, which is a recurring cycle of cold, hot, and sweating stages. During the cold stage, the patient experiences intense chills, followed by an extremely hot stage, and finally a stage of profuse sweating. Upon examination, the patient may show signs of anemia, jaundice, and have an enlarged liver and spleen, but no signs of swollen lymph nodes.

Plasmodium falciparum is the most severe form of malaria and is responsible for the majority of deaths. Severe or complicated malaria is indicated by impaired consciousness, seizures, low blood sugar, anemia, kidney damage, difficulty breathing, and spontaneous bleeding. Given the presentation, it is likely that this case involves Plasmodium falciparum.

Currently, artemisinin-based combination therapy (ACT) is recommended for treating P. falciparum malaria. This involves combining fast-acting artemisinin-based compounds with a drug from a different class. Companion drugs include lumefantrine, mefloquine, amodiaquine, sulfadoxine/pyrimethamine, piperaquine, and chlorproguanil/dapsone. Artemisinin derivatives include dihydroartemisinin, artesunate, and artemether.

If ACT is not available, oral quinine or atovaquone with proguanil hydrochloride can be used. Quinine is highly effective but not well tolerated for long-term treatment, so it should be combined with another drug, usually oral doxycycline (or clindamycin for pregnant women and young children).

Severe or complicated falciparum malaria should be managed in a high dependency unit or intensive care setting. Intravenous artesunate is recommended for all patients with severe or complicated falciparum malaria, or those at high risk of developing severe disease (such as if more than 2% of red blood cells are infected), or

To relieve the patient’s respiratory distress, the most suitable initial intervention would be positive pressure ventilation. This involves providing mechanical assistance to the patient’s breathing by delivering air or oxygen under pressure through a mask or endotracheal tube. This helps to improve oxygenation and ventilation, ensuring that the patient’s lungs are adequately supplied with oxygen and carbon dioxide is effectively removed. Positive pressure ventilation can help stabilize the patient’s breathing and alleviate the respiratory distress caused by the flail segment.

Further Reading:

Flail chest is a serious condition that occurs when multiple ribs are fractured in two or more places, causing a segment of the ribcage to no longer expand properly. This condition is typically caused by high-impact thoracic blunt trauma and is often accompanied by other significant injuries to the chest.

The main symptom of flail chest is a chest deformity, where the affected area moves in a paradoxical manner compared to the rest of the ribcage. This can cause chest pain and difficulty breathing, known as dyspnea. X-rays may also show evidence of lung contusion, indicating further damage to the chest.

In terms of management, conservative treatment is usually the first approach. This involves providing adequate pain relief and respiratory support to the patient. However, if there are associated injuries such as a pneumothorax or hemothorax, specific interventions like thoracostomy or surgery may be necessary.

Positive pressure ventilation can be used to provide internal splinting of the airways, helping to prevent atelectasis, a condition where the lungs collapse. Overall, prompt and appropriate management is crucial in order to prevent further complications and improve the patient’s outcome.