There are two answers that we can immediately rule out if we stick to the initial management of severe chest trauma: 1 (noninvasive ventilation is not indicated because it does not secure the airway) and 3 (observation in these cases, waiting for worsening, only leads to increased morbidity and mortality). Between options 2 and 4 there could be controversy between the literature and the usual clinical practice, in which we usually have to face in a delicate balance the clinical stability of the patient (and what we can "make up" this stability with our life support therapies) and the actions that result in better patient care for the definitive treatment of the lesions. We are dealing with a severe polytraumatized patient. With the data provided by the question, a patient who seems to be in shock (tachycardia, hypoxemia, tachypnea... although we do not receive data, for example, on lactacidemia), and in whom we have to our knowledge a left thoracic trauma, which not only implies bone injury, but may mask other injuries of high severity and which are not diagnosed with a chest X-ray: myocardial contusion, pericardial effusion, splenic injury, diaphragmatic injury... We place a left pleural drain on the patient and obtain a debit of 1700cc of hematic fluid. If we follow the ATLS (ATLS-Advanced Trauma Life Support 10th edition) guidelines for the care of severely polytraumatized patients, they tell us that an immediate bleeding of more than 1500cc of blood is an indication for urgent thoracotomy, and that even in patients with a bleeding of less than 1500cc, if the debit persists at a rate of 200mL/h for 2 to 4h, this indication would also exist. Therefore, the person who asked the MIR question wants us to answer option 2. However, in real life, the course of action will depend on the stability of the patient when we have applied the treatments indicated in option 2: adequate analgesia, oxygen therapy and initiation of blood transfusion. If by optimizing the patient we manage to stabilize him and assess that it is safe to transfer him, the performance of a body CT scan will define in much greater detail the lesions he has, and will help to ensure that the surgery he will probably end up undergoing will be a definitive surgery and not just damage control surgery. In this case, the doubt would arise with option 4, although, as I say, everything will depend on the clinical stability of the patient and the time we have before achieving definitive control of the hemorrhagic focus (which is, after all, what we are after in this situation).

There are two answers that we can immediately rule out if we stick to the initial management of severe chest trauma: 1 (noninvasive ventilation is not indicated because it does not secure the airway) and 3 (observation in these cases, waiting for worsening, only leads to increased morbidity and mortality). Between options 2 and 4 there could be controversy between the literature and the usual clinical practice, in which we usually have to face in a delicate balance the clinical stability of the patient (and what we can "make up" this stability with our life support therapies) and the actions that result in better patient care for the definitive treatment of the lesions. We are dealing with a severe polytraumatized patient. With the data provided by the question, a patient who seems to be in shock (tachycardia, hypoxemia, tachypnea... although we do not receive data, for example, on lactacidemia), and in whom we have to our knowledge a left thoracic trauma, which not only implies bone injury, but may mask other injuries of high severity and which are not diagnosed with a chest X-ray: myocardial contusion, pericardial effusion, splenic injury, diaphragmatic injury... We place a left pleural drain on the patient and obtain a debit of 1700cc of hematic fluid. If we follow the ATLS (ATLS-Advanced Trauma Life Support 10th edition) guidelines for the care of severely polytraumatized patients, they tell us that an immediate bleeding of more than 1500cc of blood is an indication for urgent thoracotomy, and that even in patients with a bleeding of less than 1500cc, if the debit persists at a rate of 200mL/h for 2 to 4h, this indication would also exist. Therefore, [HIDDEN]. However, in real life, the course of action will depend on the stability of the patient when we have applied the treatments indicated in [HIDDEN]: adequate analgesia, oxygen therapy and initiation of blood transfusion. If by optimizing the patient we manage to stabilize him and assess that it is safe to transfer him, the performance of a body CT scan will define in much greater detail the lesions he has, and will help to ensure that the surgery he will probably end up undergoing will be a definitive surgery and not just damage control surgery. In this case, the doubt would arise with [HIDDEN], although, as I say, everything will depend on the clinical stability of the patient and the time we have before achieving definitive control of the hemorrhagic focus (which is, after all, what we are after in this situation).

15-year-old male, admitted after being run over on the public road, resulting in being ejected. He was admitted conscious and oriented, with intense pain in the left hemithorax and dyspnea. Physical examination showed blood pressure 90/60 mmHg, heart rate 130 bpm, basal oxygen saturation 90%, respiratory rate 35 rpm. There is complete hypophonesis in the left hemithorax and dullness to percussion. Chest X-ray shows multiple left costal fractures and massive ipsilateral pleural effusion. Placement of a pleural drain is indicated, with 1700 cc of hematic fluid coming out. What is the decision to be made:

Institute noninvasive mechanical ventilation and request blood transfusion.

Analgesia, oxygen therapy, request blood transfusion and indicate urgent surgery.

Orotracheal intubation, request blood transfusion and observation for, in case of worsening, indicate surgical intervention.

Orotracheal intubation and urgent CT scan for accurate assessment of lesions.

Case 1/2013: 69-year-old male patient with sudden back and lower right limb pain and shock.

The patient, MSM, a 69-year-old man, sought medical care due to left dorsal and right lower limb pain. The chest x-ray showed mediastinal enlargement. He was undergoing examination when he lost consciousness and went into shock. Subcutaneous emphysema was observed in the left hemithorax, as well as abolition of breath sounds at auscultation. Tracheal intubation was performed with draining of blood-tinged fluid from the left hemithorax. Echocardiography showed left ventricle with 44/29 mm; septum, 12 mm; posterior wall, 13 mm; mild aortic root dilation, dissection of the lamina and periaortic hematoma. The valves and pericardium were normal. The patient was transferred to Instituto do Coraçao - InCor. Physical examination (21 Oct 2004: 10:45) showed that the patient was sedated with tracheal intubation, pale, heart rate at 90 bpm, blood pressure 130 x 80 mmHg, bloody drainage in the chest tube. Electrocardiogram - frequency 90 bpm, sinus rhythm, low voltage in the frontal plane and decreased voltage in left leads (Fig. 1). Computed tomography showed bilateral subcutaneous emphysema, thoracic aorta with inaccurate borders in its descending portion (from the subclavian artery to the middle portion), collapsed left lung and extensive collection of hematic characteristics in same hemithorax and middle and posterior mediastinum. Small right pneumothorax; small right pleural effusion with underlying parenchymal alterations. The analysis of the heart was impaired by the presence of hemothorax. While undergoing computed tomography, the patient showed no pulse, mydriasis, with asystole unresponsive to resuscitation and died (21 Oct 2011; 15:00 h).

[A case report of spontaneous hemopneumothorax].

A 55-year-old man was admitted to the private hospital with chief complaints of left chest pain and increasing dyspnea. Chest X ray on admission revealed a collapsed lung and an air fluid line in the left hemothorax. A chest tube drainage was carried out, but hemorrhagic pleural fluid of 1,000 ml was drainaged. So was the patient transferred to our hospital for surgical treatment. Following blood transfusion because of hemorrhagic pleural fluid of 1,500 ml, urgent surgery was carried out. At the operation under thoracoscope, the bleeding from the apex of the thoracic cavity was noted. The bleeding was controlled with endoscopic surgical clip. As it was, however, very difficult to remove massive blood clots under endoscopic surgery, a small thoracotomy was carried out in addition to the thoracoscopic surgery, then the bulla in the apex of left lung was resected and also removed a large amount of blood clots.

[Re-expansion pulmonary edema after emergency thoracotomy for spontaneous hemopneumothorax: a case report].

A 44-year-old man was admitted to out hospital complaining of chest pain and increasing dyspnea. Chest X-ray on admission revealed a collapsed lung and an air fluid line in the left hemothorax. Following blood transfusion because of 2,000 ml hemorrhagic pleural fluid, emergent surgery was carried out. At operation, a bleeding artery originating from the apex of the thoracic cavity and a bulla on the upper lobe were noticed. After extubation of endotracheal tube, he offered severe dyspnea with hypoxia. The chest X-ray showed figure of pulmonary edema in the left lower lobe. Patient was managed by oxygen, steroid, and urinastatin. On the 3rd operative day, pulmonary edema was disappeared. It should be kept in the mind that the re-expansion pulmonary edema occurred in patients with spontaneous hemopneumothorax of less than 3 days of duration.

[Treatment of hemopneumothorax under thoracoscopic guidance: a case report].

A 32-year-old man was admitted to our hospital complaining of chest pain and increasing dyspnea. Chest X-ray on admission revealed a collapsed lung and an air fluid line in the left hemithorax. Shock developed following drainage of 1,500 ml hemorrhagic pleural fluid. Following blood transfusion, emergency surgery was carried out. At operation under thoracoscopic guidance, a bleeding artery originating from the apex of the thoracic cavity and a bulla on the upper lobe were noted. The artery was successfully ligated with surgical clip, and the bulla was resected using EndoGIA. This case report indicates that hemopneumothorax can be safely operated on under thoracoscopic guidance after the patient has recovered from shock by adequate blood transfusion.

[Blood reflux through the catheter when trying catheterization of the subclavian vein is not a reliable sign in case of hemothorax].

A 36-year-old man suffered chest and neurovascular trauma, soft-tissue injury to the left arm, and trauma to facial bones and extremities. He was hemodynamically unstable and responded poorly to blood transfusion and vasoactive medication. Pneumothorax was suspected. When a tube was inserted into the left hemithorax, 1500 mL of blood was drained. A chest film revealed hemothorax and a contusion on the left lung, but no rib fractures. An attempt to catheterize the left subclavian vein yielded reflux, and blood was then transfused. The patient continued to be highly unstable and an additional 1000 mL of blood was drained. Exploratory thoracotomy revealed a ruptured subclavian vein, location of the venous catheter in the pleural cavity, and a fracture of the first left rib. After chest injury leading to hemothorax, reflux upon catheterization of the ipsilateral subclavian vein is not a sure sign of correct tip placement. Additional means for checking placement, such as assessing pressure wave morphology, should be used. A fracture of the first rib, which may not be evident on a chest x-ray, often causes a vascular lesion and thoracic hemorrhage. Incorrect insertion of a subclavian catheter may then follow.

Right lung complete atelectasis: an endotracheal tube displacement complication.

A 78-year-old, overweight woman with a severe individual history of the cardiovascular system was admitted in the intensive care unit with acute pulmonary edema. Despite appropriate emergency treatment, the patient did not show any clinical improvement and emergency intubation was decided. Post-intubation physical examination revealed dullness to percussion, absent breath sounds and reduced chest excursion of the right hemithorax combined with a gradual drop in blood pressure and oxygen saturation. An emergency chest X-ray showed opacification of the entire right lung and an ipsilateral shift of the mediastinum. Improvement of the patient's respiratory and hemodynamic status was observed immediately after the partial withdrawal of the tube. Tube displacement is a relative frequent complication and concerns mainly the right main bronchus due to anatomical procedures. However, the above case is a rare case of tube displacement in the left main bronchus, which led to total atelectasis of the rightlung.

[Experience on single-lung mechanical ventilation combined with damage control in treatment of patients with severe multiple trauma].

On April 6, 2020, a case of severe crush injuries in head, neck, chest and right upper extremity was admitted to Qingzhou Hospital Affiliated to the First Medical University of Shandong Province. In addition to the crush injuries, the case also suffered from shock, crush syndrome, trauma-induced coagulopathy (TIC), and acute respiratory distress syndrome (ARDS). The female patient was 44 years old, and was admitted to the hospital at 07:00 on April 6, 2020 due to traffic accident with head, neck, chest, right upper limb injuries with disturbance of consciousness for 1 hour. Admission physical examination: body temperature was 35.6 centigrade. The patient was drowsy, with swelling and cyanosis around the right orbit and right cheek. The skin was severely abraded with blood seepage. The conjunctiva was pale. The lips were slightly cyanotic. The right chest collapsed and deformed with abnormal breathing. The skin of chest wall was blue and purple with extensive feeling of holding snow under the skin. The breath sound of right lung was low and dry and wet rales could be heard. Laboratory examination: routine blood test showed that white blood cell count (WBC) was normal, red blood cell count (RBC), hemoglobin (Hb) and platelet count (PLT) decreased, blood glucose increased; urine routine examination showed glucose +++, urine occult blood +++, urinary protein +++, visible transparent and granular tube type; coagulation indicators and blood biochemical examination were abnormal. Arterial blood gas analysis showed that pH and arterial partial pressure of oxygen (PaO<sub2</sub) decreased. X-ray showed comminuted fracture of distal humerus and proximal end of right ulna and radius with dislocation of right elbow joint. CT showed swelling of soft tissue around the right orbit and depressed fracture of inner wall. After admission, single-lung ventilation, tracheotomy and prone ventilation were applied to increase oxygenation level and relieving ARDS. Fluid of damage control for resuscitation was applied to reverse shock and blood transfusion was used to control hemorrhage and TIC. According to the patient's conditions and theory of damage control surgery, right chest drainage and amputation of the right upper extremity amputation were performed in time. Then, the resection in the middle and lower part of right lung, lung repairment, and internal rib fixation were performed. Finally, selective operation was performed to cover the open wound with healing dressing, using negative pressure for suction and carrying out "stamp" skin grafting on the right chest. After treatment, the patient was out of danger, and satisfactory clinical results were achieved in the end.

InternalMed_Harrison

Difficulty in ventilation during resuscitation or high peak inspiratory pressures during mechanical ventilation strongly suggest the diagnosis. The diagnosis is made by physical examination showing an enlarged hemithorax with no breath sounds, hyperresonance to percussion, and shift of the mediastinum to the contralateral side. Tension pneumothorax must be treated as a medical emergency. If the tension in the pleural space is not relieved, the patient is likely to die from inadequate cardiac output or marked hypoxemia. A large-bore needle should be inserted into the pleural space through the second anterior intercostal space. If large amounts of gas escape from the needle after insertion, the diagnosis is confirmed. The needle should be left in place until a thoracostomy tube can be inserted.

First_Aid_Step2

If open pneumothorax is identified, an occlusive dressing must be applied immediately. This must be secured on three sides only to prevent the development of tension pneumothorax. Massive hemothorax is diagnosed through chest tube placement and is defined as > 1000 cc of immediate blood return or > 200/hour for > 2–4 hours. The treatment for massive hemothorax is volume resuscitation followed by surgery to repair the site of bleeding. The treatment for ﬂail chest is supportive, followed by surgical fixation of the chest wall. Circulation: Apply direct pressure to any actively bleeding wounds. Place a 16-gauge IV in each antecubital fossa. Isotonic ﬂuids (LR or NS) are repleted in a 3:1 ratio (ﬂuid to blood loss). Start with a ﬂuid bolus of 1–2 L in adults; then recheck vitals and continue repletion as indicated. If the patient remains tachycardic or hypotensive after the first 2 L of isotonic ﬂuid, transfusion with packed RBCs may be indicated.

Hemothorax

Ultrasound can detect blood in the pleural cavity. Blood in the thorax is shown by a uniform area without flocculation. Pleural effusions without blood are usually hypoechoic. Echogenicity is indicated by cellular debris and/or fibrin. Bloody pleural effusions are shows by a swirling, hyperechoic pattern. When a stethoscope is used (auscultation), the heartbeat sounds are faint. When percussion is performed, it produces a dull area. However, especially in traumatic cases, percussion may be painful. Although nonspecific, physical examinations may show reduced lung sounds and muffled, widespread heart sounds. Similar signs and symptoms may occur when other fluids are in the pleural cavity.

Emergency department

Asthma and COPD Acute exacerbations of chronic respiratory diseases, mainly asthma and chronic obstructive pulmonary disease (COPD), are assessed as emergencies and treated with oxygen therapy, bronchodilators, steroids or theophylline, have an urgent chest X-ray and arterial blood gases and are referred for intensive care if necessary. Noninvasive ventilation in the ED has reduced the requirement for tracheal intubation in many cases of severe exacerbations of COPD. Special facilities, training, and equipment An ED requires different equipment and different approaches than most other hospital divisions. Patients frequently arrive with unstable conditions, and so must be treated quickly. They may be unconscious, and information such as their medical history, allergies, and blood type may be unavailable. ED staff are trained to work quickly and effectively even with minimal information.

Obstructive shock

A chest X-ray can rapidly identify a pneumothorax, seen as absence of lung markings. Ultrasound can show the lack of lung sliding. However, imaging should not delay treatment. CT angiography is the standard of diagnosis of pulmonary embolism. Clots appear in the vasculature as filling defects. Treatment In any type of shock, rapid treatment is essential. Delays in therapy increase the risk of mortality. This is often done as diagnostic assessment is still occurring. Resuscitation addresses the ABC's - airway, breathing, and circulation. Supplemental oxygen is given, and intubation is performed if indicated. Intravenous fluids can increase blood pressure and maintain blood flow to organs.

[Diagnosis of pleurisy in an emergency setting].

In a medical context, it is important to precise if the pleurisy is associated with signs of tamponnade, and/or clinical presentation of ominous organic distress (acute respiratory failure, septic, haemorragic, or cardiogenic shock) or pulmonary embolism. Presence of pleural tamponnade leads to immediate decompression pleural puncture which improves rapidly in general the clinical tolerance, and later permits etiologic treatment. In more severe conditions, pleural evacuation is done in parallel with cardiopulmonary resuscitation maneuvers. If hydropneumothorax is present, immediate drainage with a chest tube will be performed. In other situations, the presence of an abundant pleural effusion with clear fluid necessitates partial needle evacuation to authorize secondarily complementary investigations with pleural biopsy. If purulent pleurisy is discovered, immediate evacuation of pus is mandatory, with needle pleural lavage or chest tube. In all cases, the pleural fluid requires complete haematological, biochemical, and cytologic as well as bacteriological analysis. In the surgical emergency ward, if an opened wound is discovered (gun shot, blunt object or weapon), cardiocirculatory resuscitation is often mandatory, with immediate transfer to the operation ward for an exploratory thoracotomy. If a closed thoracic trauma is present, the problem is generally the management of an hemo(pneumo)thorax with chest tube drainage leading sometimes if the pleural bleeding persists to thoracotomy.

Report of a lung carcinoma extended to the left atrium through pulmonary vein.

Lung cancers may extend along or grow through the pulmonary veins to invade or lie within the left atrium (LA). A 62-year-old man, previously healthy, presented with 1-month ventilatory-independent right hemithorax back pain, dry cough and large effort dyspnea. He also referred weight loss of 12 kg in 10 months and denied hemoptysis. As antecedents, he smoked for 40 years and moderate daily alcoholism. On physical examination, the patient was in good general condition, hydrated and regular respiration at rest [blood pressure (BP) =120/80 mmHg; heart rate (HR) =90 bpm; respiratory rate (RR) =16 rpm]. Cardiac auscultation revealed two standard rhythmic sounds without murmurs. Pulmonary auscultation revealed a slightly diminished vesicular murmur in the lower 1/3 of the right hemithorax without adventitious noises. Chest radiography showed a mass over the right lower lung. A CT scan confirmed the radiography image with the mass extending along the right inferior pulmonary vein and a tumor in the LA. Transthoracic and transesophageal echocardiography revealed large mass within the LA (occupying almost the entire cavity), measuring about 10 cm × 3 cm at its largest diameter, prolapsing into the left ventricle. Bronchoscopy, head CT scan, and whole-body bone scintigraphy investigation did not show any distant metastasis. The patient was successfully operated removing the intracardiac and inferior pulmonary vein tumor with the aid of cardiopulmonary bypass, followed by a right inferior lobectomy carried out after 25 days. After 30 days from surgery presented seizures associated a brain metastasis evidenced by CT when adjuvant radio and chemotherapy was started. During the next 90 days, the clinical conditions worsened, and the patient died 4 months after the surgical treatment. The case report has two primary justifications, even considering the poor outcome: (I) rarity and (II) the possibility of the surgical treatment.

[Peroperative pneumothorax in thoracotomy: the value of pulse oximetry].

Two cases of pneumothorax occurring during thoracotomy under one-lung ventilation are reported. One case occurred before pneumonectomy was carried out. The decrease in Spo2 shown by pulse oximetry, together with the increase in airway pressures, rapidly led to the diagnosis of pneumothorax. In the other case, the accident occurred after pneumonectomy, with a suddenly impossible ventilation, and a drastic decrease in Spo2 leading to hypoxic circulatory arrest. Hypoxaemia occurring during one-lung ventilation may be due to different causes. Shunting in the upper part of the lung is the main cause, but other diagnoses must be discussed, such as airway obstruction by blood or sputum, displacement of the selective endotracheal tube, bronchospasm, and pneumothorax. Monitoring of Spo2 by pulse oximetry would therefore seem to be mandatory during thoracic surgery, in order to allow an early diagnosis of hypoxaemia and speed up the treatment of its cause.

An open question.

The lungs are surrounded by the pleural membranes. The visceral pleura directly covers the lung and is separated from the parietal pleura by a layer of surfactant, which reduces friction during respiratory movement. A potential space exists between these two layers, and they may become separated by fluid or air. A lung can collapse to the size of a fist under pressure from either. Standard treatment in the field for an open chest wound is an occlusive dressing. The first thing that can be used to occlude the wound is a gloved hand. After placing the dressing, evaluate the breath sounds and determine if they have improved. The dressing should be taped down on three sides, leaving one side open to relieve the pressure during exhalation (one-way valve). "Burping" the dressing involves lifting one side to make sure any pressure buildup is relieved, as occasionally the dressing can become adhered to the skin, which may lead to a tension pneumothorax. If, after ensuring the occlusive dressing is properly in place, the respiratory rate increases, distress level worsens, oxygen saturations fall and breath sounds decrease, then needle decompression is required. A neurovascular bundle is located underneath each rib, and it is important to avoid damage to that bundle by performing a decompression over the top of a rib. If the patient is intubated before the development of a tension pneumothorax, carefully evaluate the breath sounds (especially if the left-side sounds are diminished) to determine if the ET tube needs to be withdrawn a centimeter. The rescuer performing ventilation will usually recognize a tension pneumothorax by the difficulty in bagging the patient. Remember, when you perform a needle thoracentesis, you are creating an open chest wound. Early signs and symptoms of a tension pneumothorax include diminished or absent breath sounds, severe dyspnea, narrowing pulse pressure, tachycardia and restlessness. Neck veins may be distended, but this can be a normal finding in a supine patient. The classic sign is a deviated trachea; the trachea shifts toward the "good" lung as the buildup of pressure collapses the "bad" lung. This is a late sign and suggests the tension pneumothorax has been developing for some time. One sign that does not normally accompany a plain pneumothorax is hypotension. In this case, the persistent low BP, combined with cool, mottled skin and a delayed capillary refill time, led providers to suspect that a hemothorax was developing as well. With endotracheal intubation and pleural decompression, the positive-pressure ventilations allowed the affected right lung to inflate more fully, utilize more of the available alveolar space and "bag out" some of the blood pooling at the base. The patient's vital signs and saturation improved. He needed surgical treatment and removal of the blood in the pleural space before ventilation and oxygenation could normalize.

[The effect of performance of diagnostic and therapeutic procedures on successful treatment of hemopneumothorax in isolated thoracic trauma].

Influence of performed diagnostic and therapeutic procedures on the outcome of the treatment of traumatic hemopneumothorax during isolated chest trauma. The aim of this study is the assessment of the influence of performed diagnostic and therapeutic procedures on the outcome of hemopneumothorax as a part of isolated chest trauma. The main group consists of 51 patients with hemopneumothorax. Patients with pneumothorax without effusion represent the first control group; the second control group consist of patients treated because of iatrogenic pneumothorax. In the main and control groups the analysis of clinical, roentgenographic and functional parameters was made, together with the analysis of particular therapeutic procedures, the estimation of the success of the treatment was based on roentgenographic and functional parameters. The higher incidence of hemopneumothorax compared with control groups during chest trauma in the analyzed material is statistically significant. The occurrence of bilateral hemopneumothorax in 10% of cases emphasizes the need of adequate roentgenographic assessment of injured patients. Regardless of the intensity of the trauma, symptoms do not always indicate the existence of hemopneumothorax. The number of fractured ribs is not of significant importance in terms of the occurrence of hemopneumothorax or pneumothorax. Severe dyspnea can be accompanied even with a smaller collapse of the lung independently of the amount of blood in the pleural cavity. Oxygenation in the arterial blood is impaired with the great and small pulmonary collapse. Hemodynamic disorders existed in 14% all cases. The higher frequency of operative treatment in the main group is statistically significant. The majority of cases of traumatic hemopneumothorax can be successfully treated by the conservative treatment. Accompanying complications do not have greater influence on the outcome.

Acute chest syndrome

Diagnosis The diagnosis of acute chest syndrome is made difficult by its similarity in presentation with pneumonia. Both may present with a new opacification of the lung on chest x-ray. The presence of fevers, low oxygen levels in the blood, increased respiratory rate, chest pain, and cough are also common in acute chest syndrome. Diagnostic workup includes chest x-ray, complete cell count, reticulocyte count, ECG, and blood and sputum cultures. Patients may also require additional blood tests or imaging (e.g. a CT scan) to exclude a heart attack or other pulmonary pathology. Prevention Hydroxyurea is a medication that can help to prevent acute chest syndrome. It may cause a low white blood cell count, which can predispose the person to some types of infection. Treatment Broad spectrum antibiotics to cover common infections such as Streptococcus pneumoniae and mycoplasma, pain control, and blood transfusion. Acute chest syndrome is an indication for exchange transfusion.

Explosive pleuritis.

The objective of the present paper is to describe the clinical and computed tomography features of 'explosive pleuritis', an entity first named by Braman and Donat in 1986, and to propose a case definition. A case report of a previously healthy, 45-year-old man admitted to hospital with acute onset pleuritic chest pain is presented. The patient arrived at the emergency room at 15:00 in mild respiratory distress; the initial chest x-ray revealed a small right lower lobe effusion. The subsequent clinical course in hospital was dramatic. Within 18 h of admission, he developed severe respiratory distress with oxygen desaturation to 83% on room air and dullness of the right lung field. A repeat chest x-ray, taken the morning after admission, revealed complete opacification of the right hemithorax. A computed tomography scan of the thorax demonstrated a massive pleural effusion with compression of pulmonary tissue and mediastinal shift. Pleural fluid biochemical analysis revealed the following concentrations: glucose 3.5 mmol/L, lactate dehydrogenase 1550 U/L, protein 56.98 g/L, amylase 68 U/L and white blood cell count 600 cells/mL. The pleural fluid cultures demonstrated light growth of coagulase-negative staphylococcus and viridans streptococcus, and very light growth of Candida albicans. Cytology was negative for malignant cells. Thoracotomy was performed, which demonstrated a loculated parapneumonic effusion that required decortication. The patient responded favourably to the empirical administration of intravenous levofloxacin and ceftriaxone, and conservative surgical methods in the management of the empyema. This report also discusses the patient's rapidly progressing pleural effusion and offers a potential case definition for explosive pleuritis. Explosive pleuritis is a medical emergency defined by the rapid development of a pleural effusion involving more than 90% of the hemithorax over 24 h, which causes compression of pulmonary tissue and mediastinal shift to the contralateral side.

Emergency thoracotomies: Two center study.

Emergency thoracotomy is performed either immediately at the scene of injury, in the emergency department or in the operating room. It aims to evacuate the pericardial tamponade, control the haemorrhage, to ease the open cardiac massage and to cross-clamp the descending thoracic aorta to redistribute blood flow and maybe to limit sub-diaphragmatic haemorrhage, bleeding and iatrogenic injury are the common risk factors. We aimed to review our experience in the field of emergency thoracotomies, identify the predictors of death, analyze the early results, detect the risk factors and asses the mortalities and their risk factors. Our hospital records of 197 patients who underwent emergency thoracotomy were reviewed. We retrospectively analyzed a piece of the extensive experience of the Mansoura University Hospitals and Mansoura Emergency Hospital; Egypt and Saudi German Hospitals; Jeddah in the last 12 years in the management of trauma cases for whom emergency thoracotomy. The aim was to analyse the early results of such cases and to detect the risk factors of dismal prognosis. Our series included 197 cases of emergency thoractomies in Mansoura; Egypt and SGH; Jeddah; KSA in the last 12 years. The mean age of the victims was 28 years and ranged between 5 and 62 years. Of the 197 patients with emergency thoracotomy, the indications were both penetrating and blunt chest trauma, iatrogenic and postoperative hemodynamito a surgical cause. The commonest indication was stab heart followed by traumatic diaphragmatic ruptures. The results of emergency thoracotomy in our series were cooping with the results of other reports, mainly due to our aggressive measures to achieve rapid stabilization of the hemodynamic condition. We emphasize the importance of emergency medicine education programs on rapid diagnosis of traumatic injuries with early intervention, and adequate hemodynamic and respiratory support. Emergency thoracotomy has an important role in emergency big volume hospitals and can save a lot of lives. Outcome can be improved by increasing the learning curve and the integrated cooperation of the emergency and surgical teams.

Transfusion associated circulatory overload

The management of TACO includes immediate discontinuation of the transfusion, supplemental oxygen if needed, and medication to remove excess fluid. Symptoms and signs The primary symptoms of TACO are signs of respiratory distress (shortness of breath, low oxygen levels in the blood) along with signs of excess fluid within the circulatory system (leg swelling, high blood pressure, and an elevated heart rate). On physical exam, patients may present with crackles when listening to the lungs, a murmur (S-3 murmur) when listening to the heart, leg swelling, and distended veins in the neck (jugular venous distension).

Transfusion-related acute lung injury

Transfusion-related acute lung injury (TRALI) is the serious complication of transfusion of blood products that is characterized by the rapid onset of excess fluid in the lungs. It can cause dangerous drops in the supply of oxygen to body tissues. Although changes in transfusion practices have reduced the incidence of TRALI, it was the leading cause of transfusion-related deaths in the United States from fiscal year 2008 through fiscal year 2012. Signs and symptoms It is often impossible to distinguish TRALI from acute respiratory distress syndrome (ARDS). The typical presentation of TRALI is the sudden development of shortness of breath, severe hypoxemia (O2 saturation <90% in room air), low blood pressure, and fever that develop within 6 hours after transfusion and usually resolve with supportive care within 48 to 96 hours. Although low blood pressure is considered one of the important signs for diagnosing TRALI, in some cases high blood pressure can occur.

Dabigatran-Induced Massive Spontaneous Hemothorax.

Spontaneous hemothorax due to anticoagulant use is extremely rare in clinical practice. Dabigatran is a novel anticoagulant to prevent stroke or thromboembolic episodes in patients with nonvalvular atrial fibrillation. We report on an 83-year-old man who received dabigatran therapy (110 mg twice daily) for 7 months and developed massive spontaneous hemothorax and acute renal failure. The patient was admitted to the hospital with complaint of a dull ache in the chest and dyspnea. Chest computed tomography scan revealed massive pleural effusion in the left hemithorax with atelectasis. Acute renal failure was observed 4 days later after admission. Almost 2500 mL of blood was repeatedly drained by ultrasound-guided thoracocentesis, followed by a dramatic decrease in serum red blood cell count, hemoglobin and hematocrit. After excluding other possible causes, diagnostic withdrawal was performed for dabigatran, and plasma transfusion was conducted to supply the lost blood volume. A causal relationship was established, because the patient's renal function gradually improved and no further pleural effusion developed after dabigatran was discontinued. This is a rare case report of massive spontaneous hemothorax caused by dabigatran. Therefore, practitioners should be aware of hemothorax as a potential complication of dabigatran therapy.

[A case of spontaneous hemopneumothorax occurred after thoracocentesis].

A 41-year-old man was admitted to our hospital complaining of severe right chest pain and dyspnea. Soon after, right thoracocentesis was done and pleural free air was aspirated. Twenty minutes later he fell into a shock status. Chest roentgenogram showed massive right pleural fluid collection. Chest drainage revealed that massive bleeding continued. Therefore, emergent thoracotomy was performed. Bleeding point was a ruptured stump of pleural adhesion of the apical parietal pleura. His postoperative course was almost good, and discharged on the tenth postoperative day. Careful observation after thoracic aspiration is necessary in the treatment of spontaneous pneumothorax.

Multiloculated pleural effusion detected by ultrasound only in a critically-ill patient.

Multiloculated pleural effusion is a life-threatening condition that needs early recognition. Drainage by chest tube might be difficult which necessitates a surgical intervention. While x-ray typically does not show loculations, CT scan might not also identify the loculations. Ultrasound has a high sensitivity in detecting pleural diseases including multiloculated pleural effusion. A 55-year-old female presented with dyspnea, cough and yellowish sputum for 3 days. Her heart rate was 136 bpm ,O2 saturation 88%, and WBC 21,000/mcL. Chest x-ray showed complete opacification of right lung. A chest tube insertion was unsuccessful. CT scan of the chest showed large pleural effusion occupying the right hemithorax with collapse of the right lung. Bedside ultra-sound showed a multiloculated pleural effusion with septations of different thickness. The patient subsequently underwent thoracotomy which showed multiple, fluid-filled loculations with significant adhesions. The loculations were dissected along with decortications of thick a pleural rind. Blood and pleural fluid cultures grew Streptococcus pneumoniae and the patient was treated successfully with Penicillin G. We advocate bedside ultrasound in patients with complete or near complete opacification of a hemithorax on chest x-ray. CT scan is less likely to show septations within pleural effusions compared to ultrasounnd. Therefore, CT scan and ultrasound are complementary for the diagnosis of empyema and multiloculated pleural effusion.

[Hemothorax].

Hemothorax is defined as blood accumulation in the pleural cavity with a hematocrit value of the effusion exceeding 50%. Symptoms and severity vary, ranging from asymptomatic to an imminent state of threatened cardiac arrest. This paper presents the etiology, initial work-up, and treatment of hemothorax, with an emphasis on massive hemothorax requiring an emergent thoracotomy for hemostasis. The etiology of hemothorax can be traumatic, iatrogenic, and non-traumatic/non-iatrogenic. Regardless of the etiology, the initial medical examination should be performed as in the initial trauma examination to evaluate the urgency, the amount of bleeding in the chest cavity, and the coexistence of pneumothorax. If massive hemothorax or tension pneumothorax is present, thoracic tube drainage should be started immediately. Contrast-enhanced computed tomography (CT) should be performed to identify the source of bleeding. Treatment includes fluid and blood transfusions to stabilize the circulation. Anticoagulants and antiplatelet agents should be neutralized, reduced, or withdrawn. Emergent thoracotomy for hemostasis is indicated for massive hemothorax with unstable circulation. Anterior-parasternal thoracotomy performed in the supine position has the advantage of rapid thoracotomy and good visualization. Endovascular therapy is effective when contrast-enhanced CT identifies the source of bleeding.

[Diagnosis and treatment of parapneumonic effusions--case 10/2009].

We report on a 47-year-old male patient who was admitted for exercise-induced dyspnea and easy fatigability. Physical examination revealed reduced breath and percussion sounds of the left basal lung. Laboratory investigations revealed leucocytosis and elevated C-reactive protein levels. Chest X-ray showed an area of increased opacity of the left lower hemithorax. Computed tomography (CT) confirmed an encapsulated, septated pleural effusion. The aspirate was purulent with abundant neutrophil granulocytes and a pH value of 7.1. A diagnosis of left-sided pleural empyema was made, most probably following pneumonia. Antibiotic treatment with amoxicillin and clavulan acid was initiated and after insertion of a chest drain pleural irrigation with daily 200,000 I.U. streptokinase was performed for five days. The drainage was removed after ten days and after four months CT showed a complete remission of the lef-sided pleural empyema. Parapneumonic effusions are frequent with broad clinical range from trivial to life-threatening. Therapy decision is based on the characteristics of the effusion and the patient's clinical status and should be made within an interdisciplinary cooperation between internists and (thoracic) surgeons.

[Treatment indication with endothoracic drainage tube in parapneumonic effusions by partial pressure of carbon dioxide measurement in pleural fluid].

Parapneumonic effusions with pH < 7.20 or glucose < 0.40 g/l or lactate dehydrogenase (LDH) > 1000 U/l have indication of treatment with endothoracic drainage tube (EDT). The aim of the present study was to determine the accuracy of partial pressure of carbon dioxide (pCO2) measurement in pleural fluid for the subsequent treatment indication with EDT in parapneumonic effusions, by analyzing the area under curve ROC (AUC) and determining the optimal cut off value. 207 pleural fluids were studied. Glucose, LDH, pCO2, and pH were measured, and data concerning the etiology of pleural effusion and whether EDT treatment was needed were collected after patients were discharged from hospital. Forty-six out of 207 pleural fluids studied were parapneumonic effusions. Thirty-two were treated with EDT. AUC values were 0.888 (p < 0.0001), 0.890 (p < 0.0001), 0.816 (p < 0.0001), and 0.801 (p < 0.0001) for pCO2, pH, glucose, and LDH, respectively. No significant differences were found among them. Optimal cut off value for pCO2 was 48.6 mmHg, exhibiting 90.6% sensitivity and 78.6% specificity. All parapneumonic effusions showing pCO2 > 60.9 mmHg were treated with EDT. Remarkably, 3 out of 46 parapneumonic effusions (6.5%) that had been improperly treated following pH, glucose or LDH values, were correctly treated following pCO2. pCO2 determination in pleural fluid appears to be the best way to decide the indication of EDT in parapneumonic effusions.

A large pericardial cystic lymphangioma presenting as acute-onset respiratory distress in a child: a case report.

Lymphangiomas are rare benign malformations of the lymphatics that occur due to blockage of the lymphatic system during fetal development. They commonly occur in the neck and axilla, while involvement of the pericardium is rare. We report herein the case of a 16-month-old Sri Lankan child with a large pericardial cystic lymphangioma presenting with sudden-onset shortness of breath. A 16-month-old Sri Lankan boy presented with sudden-onset dyspnea for 1-day duration following a febrile illness that lasted 2 days. On examination, he was afebrile and had subcostal, intercostal, and suprasternal recessions, with a respiratory rate of 50 breaths per minute. He had a loud expiratory grunt. The chest expansion was reduced on the right side, which was dull to percussion. Auscultation revealed a marked reduction of air entry over the right lower and mid zones. Chest X-ray showed a well-demarcated opacity involving the lower and mid zones of the right hemithorax associated with a tracheal shift to the opposite side. Ultrasound scan of the chest revealed fluid-filled right hemithorax suggesting a septate pleural effusion. A contrast-enhanced computed tomography scan of the thorax showed a large multiloculated extrapulmonary cystic lesion involving the right hemithorax with a mediastinal shift towards the left side associated with displacement of the right-side mediastinal structures. He underwent mini-thoracotomy and surgical excision of the cyst. A large cyst originating from the pericardium was observed and excised during surgery. Histological examination revealed a lesion composed of cysts devoid of a lining epithelium but separated by connective tissue, mature adipose tissue, and lymphoid aggregates. The child showed complete recovery postoperatively with full expansion of the ipsilateral lung. We report the case of a patient with cystic lymphangioma who was perfectly well and asymptomatic until 16 months of age. This case report presents the very rare occurrence of a large cystic lymphangioma originating from the pericardium. It highlights the importance of considering rare possibilities and performing prompt imaging in situations of diagnostic uncertainty to arrive at an accurate diagnosis that can be lifesaving.

Airway obstruction during pneumonectomy using a single lumen tube: A case report.

Endotracheal intubation is an essential step for airway management during general anesthesia. When surgeons carry out thoracic surgery such as pneumonectomy, they usually request lung isolation to secure a clear surgical view. A double lumen endotracheal tube is used for lung isolation in routine thoracic surgeries. A 56-year-old man was previously diagnosed with left Aspergilloma, a tuberculosis destroyed lung, and diabetes mellitus. According to his chest x-ray and chest computed tomography, his left lung was nearly collapsed, and the result of a pulmonary function test was severely restricted. The patient's diffusing capacity for carbon monoxide was 63% and predicted postoperative forced expiratory volume in 1 second was 23.5% DIAGNOSES:: Due to his previous history, radiologic findings and laboratory test results, he was diagnosed with left Aspergilloma and tuberculosis destroyed lung. Due to recurrence of Aspergilloma in his left lung, the patient was scheduled for a left pneumonectomy. Since the patient's partial oxygen concentration was adequate despite his left lung being nearly totally collapsed, we thought that we would be capable of performing the pneumonectomy using a single lumen tube (SLT). For a better surgical view, we planned lung isolation via insertion of a SLT deep into the bronchus. During pneumonectomy, after tracheal suction was performed, we tried a lung recruitment maneuver. Suddenly end-tidal carbon dioxide did not show on the monitor. The patient's blood pressure dropped and heart rate was decreasing. We thought that cardiopulmonary resuscitation was needed and an approximately 2 cm sized hematoma was removed from the endotracheal tube after vigorous suctioning. After getting rid of the hematoma, we changed the single tube to a double lumen tube (DLT). This case led us to the conclusion that a DLT should be used for safety when carrying out thoracic surgery. We report a rare case of an airway obstruction using a SLT during pneumonectomy.

Spontaneous haemopneumothorax.

An 18-year-old man presented with a 2 day history of breathlessness and left-sided chest pain, with no preceding trauma. He had no medical history of note, and had never smoked. He was in hypovolaemic shock, with Hb of 8.1 g/dl, and received fluid resuscitation. Chest x-ray (CXR) revealed left-sided hydropneumothorax, with the effusion of blood-consistency on CT thorax. Tube thoracostomy drained 1.7 litres of blood immediately. He remained haemodynamically stable after 4 units of blood transfusion on the first day with post-transfusion Hb 11 g/dl. Following cardiothoracic surgeon advice, tube was removed on day 5 draining total of 3.5 litres, with good response clinically and radiologically. Patient was well when followed up at 1 week after hospital discharge, with no recurrence and complete re-expansion of left lung on CXR.

[Anesthesia in obstetric patient with sickle cell anemia and thalassemic trait after plasmapheresis: case report].

Plasmapheresis is the technique of choice for severe hemolytic anemia patients. A consequence is plasma cholinesterase depletion, which interferes with metabolism of some neuromuscular blockers currently used in anesthesiology. Pregnant patient, 26 years old, physical status ASA IV, 30 weeks and 3 days gestational age, with sickle cell anemia, thalassemic trait and allo-immunization for high frequency antigens. Patient presented sickling crisis being transfused with incompatible blood. Patient evolved with massive hemolysis being admitted with 3 g/dL hemoglobin and 10% hematocrit, severe jaundice, tachycardia, apathic and pale. Hematological evaluation has concluded for the inexistence of compatible blood for transfusion. Patient was treated with steroids, immunoglobulins and plasmapheresis. In the second admission day patient evolved with acute renal failure and pulmonary edema, general state worsening and hemodynamic instability. Gestation resolution was indicated due to patient's clinical conditions and consequent acute fetal suffering. Patient was admitted to the operating room conscious, pale, with dyspnea, jaundice, 91% SpO2 in room air, heart rate of 110 bpm and blood pressure of 110 x 70 mmHg, under dopamine (1 microg.kg-1.min-1) and dobutamine (10 microg.kg-1.min-1). We decided for balanced general anesthesia with alfentanil (2.5 mg), etomidate (14 mg), atracurium (35 mg) and isoflurane. There were no anesthetic-surgical intercurrences. Patient was referred to ICU after surgery completion under tracheal intubation and vasoactive drugs, being extubated 3 hours later. This case was a challenge for the team since patient was hemodynamically instable with coagulogram abnormalities counterindicating regional anesthesia. In addition, plasmapheresis potentially depletes plasma cholinesterase reserves, interfering with anesthesia. However, available drug armamentarium has allowed for the safe management of this situation.


She is going to have myeloma. For diagnosis, a sample (bone marrow) and electrophoresis to determine the type of monoclonal peak. Then, for extension, prognostic value and to decide treatments, the rest, but once diagnosed.

A 72-year-old man comes to the Emergency Department with a pathological fracture of the left femur. After surgery, a diagnostic study is performed to determine the underlying pathology with the following findings: hemoglobin 9.5 g/dl, total proteins 11 g/dl, (VN: 6-8 g/dl), serum albumin 2 g/dl, (VN 3.5-5.0 g/dl), beta 2 microglobulin 6 mg/l (VN 1.1-2.4 mg/l), serum creatinine 1.8 mg/dl (VN: 0.1-1.4 mg/dl). Indicate which diagnostic tests would be necessary to confirm the most likely diagnosis:

Radiological bone series and bone marrow aspirate.

Serum and urine electrophoresis and renal function tests.

Bone marrow aspirate and serum calcium concentration.

Bone marrow aspirate and serum and urine electrophoresis.

Biopsy of the pathological fracture and radiological bone series.

Approach to the treatment of the older, unfit patient with myeloma from diagnosis to relapse: perspectives of a US hematologist and a geriatric hematologist.

Mrs. A. is a 73-year-old woman who has developed increasing fatigue and lower back pain over the past year. The pain limits her exercise tolerance such that she can now walk only 1 block. She is a retired schoolteacher who does volunteer efforts in her community but has limited her activities due to fatigue. Karnofsky performance status is 70%. She has a history of chronic hypertension treated with a diuretic, adult-onset diabetes mellitus treated with metformin, and hypothyroidism treated with levothyroxine. Initial evaluation reveals anemia, renal dysfunction, an elevated total protein, and an L2 compression fracture on lumbosacral radiographs. Results of initial and subsequent evaluation are shown below, and she is referred to a hematologist for further evaluation, which revealed the following: calcium 9.0 mg/dL, creatinine 3.2 mg/dL with estimated creatinine clearance using the Modification of Diet in Renal Disease equation of 15 mL/min, hemoglobin 9.6 g/dL, total protein 11 g/dL, albumin 3.2 g/dL, immunoglobulin A (IgA) λ M protein 6.8 g/dL, total IgA 7.2 g/dL, IgG 0.4g/dL, IgM 0.03 g/dL, free κ <0.01 mg/L, free λ 1000 mg/L, serum free light chain ratio <0.01, β-2-microglobulin 4.2, viscosity 3.0, lactate dehydrogenase 200 U/L, urine protein electrophoresis: 125 mg/dL with 30% M protein, and urine immunofixation: λ light chain. Skeletal bone survey showed lytic lesions in femurs and humeri and diffusely in ribs bilaterally as well as compression fractures at T4, T6, and L2. Bone marrow biopsy revealed λ-restricted plasma cells comprising 50% of the bone marrow core. Fluorescence in situ hybridization testing on marrow showed that del 17p was present in 80% of the plasma cells. Mrs. A. is informed of the diagnosis of multiple myeloma and the need for therapy. She requests consultation with 2 of the leading world experts. However, she wants to be treated near her home and does not want treatment on a clinical trial.

Treatment of Relapsed Myeloma in a Patient With Renal Insufficiency.

The Oncology Grand Rounds series is designed to place original reports published in the Journal into clinical context. A case presentation is followed by a description of diagnostic and management challenges, a review of the relevant literature, and a summary of the authors' suggested management approaches. The goal of this series is to help readers better understand how to apply the results of key studies, including those published in Journal of Clinical Oncology, to patients seen in their own clinical practice. A 45-year-old man was diagnosed in March 2010 with stage III immunoglobulin G kappa multiple myeloma (MM) after presenting with bone pain as a result of multiple lytic bone lesions and T12 vertebral collapse. Laboratory work-up showed a serum M protein of 72 g/L and a 24-hour kappa light-chain urine protein excretion of 730 mg, hemoglobin of 10.2 g/dL, serum albumin of 49 g/L, serum β<sub2</sub-microglobulin of 6.4 mg/L, serum creatinine level of 1.6 mg/dL with an estimated glomerular filtration rate (eGFR) of 47 mL/min/1.73 m<sup2</sup, and normal serum calcium and lactate dehydrogenase (LDH) levels. His bone marrow contained 58% plasma cells, which showed the 17p deletion abnormality (Fig 1). He was treated with vertebroplasty and alternating chemotherapy with carmustine, vincristine, cyclophosphamide, melphalan, and prednisone and vincristine, carmustine, doxorubicin and dexamethasone. Because of progressive disease, salvage therapy with bortezomib and dexamethasone was administered with no response. The patient was then switched to lenalidomide and dexamethasone, which yielded minimal response. He underwent autologous stem-cell transplantation (ASCT) with melphalan 200 mg/m<sup2</sup as high-dose therapy in February 2011, which led to a partial response, but in December 2011, progressive disease was documented, and the patient was enrolled in a clinical trial of carfilzomib monotherapy, with stable disease for 33 cycles. In October 2014 serum M protein rose to 38.6 g/L, with 24-hour kappa light-chain urine protein excretion of 840 mg, serum creatinine of 2.1 mg/dL, and an eGFR of 41 mL/min/1.73 m<sup2</sup. He presented to discuss ongoing treatment options.

Biclonal gammopathy in multiple myeloma: a case report.

Monoclonal gammopathy is a group of B-cell disorders which result in the production of a specific and unique monoclonal immunoglobulin (M-component). Biclonal gammopathy is characterized by the simultaneous appearance of two different M-components. The incidence is about 1% of all monoclonal gammopathy. This paper reports on a 48-year-old male who had a chief complaint of back-pain beginning 7 months earlier. A physical examination was unremarkable, except for anemia and tenderness in the back. Hemoglobin was 5.4 g/dl, white blood cells 4.5 x 10(3)/microliter, platelets 157 x 10(3)/microliter, and reticulocytes 0.9%. Serum iron was 79 mg/dl, and total iron-binding capacity was 210 mg/dl. A blood smear showed the formation of rouleaux, but no plasma cells were found. Serum creatinine was 5.4 mg/dl, with a creatinine clearance of 18.1 ml/min. Serum electrolytes were normal except for serum calcium which was 14.4 mg/dl. The urinalysis showed strongly positive proteinuria (+2), with negative Bence Jones protein. Serum protein electrophoresis showed an increase and a spike pattern of beta-2 globulin (2.8 g/dl) and alpha-2 globulin (1.5 g/dl), with normal gamma globulin. By nephelometry technique, serum IgG was normal (1388 mg/dl), IgA was high (900 mg/dl), and IgM was also high (517 mg/dl). Advanced and extensive osteolytic lesions were found in the clavicle, ribs, skull, humerus, femur, and columna vertebralis. Plasma cells (myeloma cells) in bone marrow were 32%. The clinical diagnosis was multiple myeloma (biclonal gammopathy) stage IIIB (Durie and Salmon staging system). Clinical response was good after two series of conventional chemotherapy, with normal serum electrophoresis, decreasing serum creatinine and serum calcium. Based on the above data, the diagnosis of multiple myeloma with biclonal gammopathy was confirmed. This is a rare case with a combination of IgA and IgM M-components.

Multiple myeloma

Diagnostic criteria In 2003, the IMG agreed on diagnostic criteria for symptomatic myeloma, asymptomatic myeloma, and MGUS, which was subsequently updated in 2009: Symptomatic myeloma (all three criteria must be met): Clonal plasma cells >10% on bone marrow biopsy or (in any quantity) in a biopsy from other tissues (plasmacytoma) A monoclonal protein (myeloma protein) in either serum or urine and it has to be more than 3g/dL (except in cases of true nonsecretory myeloma) Evidence of end-organ damage felt related to the plasma cell disorder (related organ or tissue impairment, CRAB): HyperCalcemia (corrected calcium >2.75 mmol/l, >11 mg/dl) Renal failure (kidney insufficiency) attributable to myeloma Anemia (hemoglobin <10 g/dl) Bone lesions (lytic lesions or osteoporosis with compression fractures)

Should bone marrow examination be routinely performed for the diagnosis of monoclonal gammopathy of undetermined significance?

Monoclonal gammopathy of undetermined significance is defined by the presence of: low serum and/or urine monoclonal protein level; less than 10% plasma cells in bone marrow; normal serum calcium, creatinine and hemoglobinlevels; and no bone lesions on full skeletal X-ray survey. To study the necessity of bone marrow examination for the diagnosis and clinical course of MGUS. We retrospectively screened the medical records of all patients in whom monoclonal protein was found in the serum during 2001-2002 in the medical laboratories of Meir Medical Center. Asymptomatic patients who had serum monoclonal immunoglobulin G < 3.0 g/dl or IgA < 2.0 g/dl or IgM < 1.0 g/dl without anemia, renal failure, hypercalcemia or any bone lesions on skeletal survey were eligible. Full records of patients who were evaluated in the hematology clinic were available (group 1). The remaining patients were followed by their family physicians; thus we had access only to their electronic files including laboratory results and new diagnoses (group 2). Demographic and clinical parameters as well as clinical course werewere evaluated. Both groups (57 and 255 patients, respectively) had similar demographic, laboratory and clinical characteristics. Bone marrow examination was performed in 30 of 57 patients (group 1): 16 were normal, 8 had an excess of normal plasma cells, and 6 had excess of pathologic plasma cells. However, only in two of the latter six could a diagnosis of multiple myeloma be established. All group 1 patients were followed for 22 +/- 11 months and onlytwo developed overt multiple myeloma. During the same period, 6 of 255 patients (group 2) were diagnosed as multiple myeloma and 3 as MGUS in other hospitals. The rest had a stable course with no change in their laboratory values. Our findings suggest that bone marrow examination should not be performed routinely in patients who fulfill strict clinical and laboratory criteria of MGUS.

Multiple Myeloma -- Evaluation

Historically, we have diagnosed MM if clonal bone marrow plasma cells were greater than or equal than 10% on bone marrow biopsy (or if a biopsy-proven plasmacytoma was present) in addition to at least one of the following CRAB criteria: Serum calcium level greater than 0.25 mmol/L (greater than 1 mg/dL) higher than the upper limit of normal or greater than 2.75 mmol/L (greater than 11 mg/dL) Renal insufficiency (creatinine greater than 2 mg/dL [greater than 177 micromol/L] or creatinine clearance less than 40 mL per minute) Anemia (hemoglobin less than 10 g/dL or hemoglobin greater than 2 g/dL below the lower limit of normal) One or more osteolytic bone lesions on skeletal radiography, CT, or PET-CT often described as punched-out, round, radiolucent lesions

Treatment approach for the older, unfit patient with myeloma from diagnosis to relapse: perspectives of a European hematologist.

Mrs. A. is a 73-year-old woman who has developed increasing fatigue and lower back pain over the past year. The pain limits her exercise tolerance such that she can now walk only 1 block. She is a retired schoolteacher who does volunteer efforts in her community but has limited her activities due to fatigue. Karnofsky performance status is 70%. She has a history of chronic hypertension treated with a diuretic, adult-onset diabetes mellitus treated with metformin, and hypothyroidism treated with levothyroxine. Initial evaluation reveals anemia, renal dysfunction, an elevated total protein, and an L2 compression fracture on lumbosacral radiographs. Results of initial and subsequent evaluation are shown below, and she is referred to a hematologist for further evaluation, which revealed the following: calcium 9.0 mg/dL, creatinine 3.2 mg/dL with estimated creatinine clearance using the Modification of Diet in Renal Disease equation of 15 mL/min, hemoglobin 9.6 g/dL, total protein 11 g/dL, albumin 3.2 g/dL, immunoglobulin A (IgA) λ M protein 6.8 g/dL, total IgA 7.2 g/dL, IgG 0.4 g/dL, IgM 0.03 g/dL, free κ <0.01 mg/L, free λ 1000 mg/L, free light chain ratio <0.01, β-2-microglobulin 4.2, viscosity 3.0, lactate dehydrogenase 200 U/L, urine protein electrophoresis: 125 mg/dL with 30% M protein, and urine immuno-electrophoresis: λ light chain. Skeletal bone survey showed lytic lesions in femurs and humeri and diffusely in ribs bilaterally as well as compression fractures at T4, T6, and L2. Bone marrow biopsy revealed λ-restricted plasma cells comprising 50% of the bone marrow core. Fluorescence in situ hybridization testing on marrow showed that del(17p) was present in 80% of the plasma cells. Mrs. A. is informed of the diagnosis of multiple myeloma and the need for therapy. She requests consultation with 2 of the leading world experts. However, she wants to be treated near her home and does not want treatment on a clinical trial.

Multiple myeloma

Signs and symptoms Because many organs can be affected by myeloma, the symptoms and signs vary greatly. Fatigue and bone pain are the most common symptoms at presentation. The CRAB criteria encompass the most common signs of multiple myeloma: Calcium: serum calcium >0.25 mmol/l (>1 mg/dl) higher than the upper limit of normal or >2.75 mmol/l (>11 mg/dl) Renal insufficiency: creatinine clearance <40 ml per minute or serum creatinine >1.77 mol/l (>2 mg/dl) Anemia: hemoglobin value of >2g/dl below the lowest limit of normal, or a hemoglobin value <10g/dl Bone lesions: osteolytic lesions on skeletal radiography, CT, or PET/CT Bone pain

[Nonproducing myeloma without evident bone lesion].

A 76-year-old female was admitted to our hospital because of anemia. Complete blood count was as follows: RBC 2.37 X 10(6)/microliters, Hb 7.7 g/dl, WBC 2,600/microliters, Plt 105 X 10(3)/microliters. A bone marrow aspirate revealed 40.8% plasmacytoid cells showing the characteristics of plasma cells by electron microscopy. Total serum protein was 5.4 g/dl. Monoclonal protein was not observed by electrophoresis. On immunoelectrophoresis, M-bow was not observed in the serum or in 50-fold concentrated urine. The plasma cells were negative for cytoplasmic IgG, M, A, E, D, kappa or lambda by immunoperoxidase studies. Although radiologic studies of the bones did not reveal destructive or punched out lesions, we diagnosed this case as a nonproducing myeloma and the patient responded to MP therapy. This case was considered interesting as regards the pathological entity of myeloma.

[An autopsy case of IgE myeloma].

An autopsy case of IgE myeloma, 85-year-old male is reported. He was admitted to our hospital on November 17, 1987 due to pain of left humerus. Osteolytic and osteoporotic foci were found in left humerus, ribs, spinal column and femurs. Complete blood countings were as follows: RBC 3.23 x 10(12)/L, Hb 11.3 g/dl, WBC 6.3 x 10(9)/L, platelet 173 x 10(9)/L. Blood smear showed red cell rouleaux formation without myeloma cells. Examination of bone marrow revealed hypoplasia with 52% myeloma cells which were stained with anti-IgE and antilambda antisera by peroxidase anti-peroxidase method. Total serum protein level was 7.7 g/dl. Monoclonal protein was observed at fast gamma-region by cellulose-acetate electrophoresis. On immunoelectrophoresis, this monoclonal protein made specific M-bow against anti-IgE and anti-lambda antisera. The IgE level in serum and urine were 7.8 x 10(6) IU/ml and 2.4 x 10(3) IU/ml by radio-immunoassay respectively. He was died owing to renal failure on September 7, 1988. Postmortem examination showed infiltration of myeloma cells in bone marrow, spleen, kidneys, lungs and generalized lymph nodes.

Spurious hyperphosphatemia in a case of multiple myeloma.

A 50 year old male was admitted in our hospital with anemia and impaired renal function. He was subsequently found to have extremely elevated serum phosphate level (24 mg/dL, reference interval: 2.5-4.5 mg/dL) with normal serum calcium when assayed on a Beckman Coulter AU 480(®) analyser. Clinico-biochemical discrepancy led to the suspicion of spurious hyperphosphatemia. Serum total protein was grossly elevated with gross reversal of albumin to globulin ratio. Serum electrophoresis revealed a large M band and was confirmed as Ig G-Kappa type on immunofixation. Subsequently a bone marrow aspiration biopsy confirmed the diagnosis of multiple myeloma. The patient serum was then reassayed for phosphate on a Vitros(®) 250 Dry Chemistry platform and the result was within normal reference interval. Paraproteinemias are a common cause of analytical interference in clinical biochemistry laboratories and as multilayered film technology platforms like Vitros(®) assay most routine analytes on a protein free filtrate they are unaffected by paraprotein interference. Clinically discordant patient results should always be interpreted keeping such interferences in mind.

Primary hyperparathyroidism

Serum calcium concentration of 1.0 mg/dL (0.25 mmol/L) or more above the upper limit of normal Creatinine clearance that is reduced to <60 mL/min Bone density at the hip, lumbar spine, or distal radius that is more than 2.5 standard deviations below peak bone mass (T score <-2.5) and/or previous fragility fracture Age less than 50 years

Atypical sarcoidosis diagnosed by bone marrow biopsy during renal workup for possible multiple myeloma.

Sarcoidosis is a multi-organ disease of unknown etiology characterized by non-caseating granulomas. Here we report the case of a 78-year-old white male with a past medical history of diabetes mellitus, hypertension, and chronic kidney disease stage III with a baseline serum creatinine of 2.5 mg/dl. The patient had a prior admission history for acute kidney injury (AKI) attributed to dehydration and medication-induced nephro-toxicities. He presented to the renal clinic for follow-up with acute worsening of chronic kidney failure with a serum creatinine level of 3.5 mg/dl. Examination revealed that he was anemic and mildly hypercalcemic with suppressed parathyroid hormone and had proteinuria of 1.3 g per day. The computed tomography scan of the abdomen revealed right renal pelvic non-obstructing calculi. Serum protein electrophoresis revealed gammopathy with two distinct monoclonal peaks consisting of immunoglobulin G (IgG) kappa and IgG lambda, respectively. The kappa/lambda ratio was within normal limits, and urine protein electrophoresis showed no evidence of a monoclonal peak or Bence Jones proteins. Further workup for multiple myeloma, including bone marrow (BM) biopsy, revealed polyclonal plasma cells and B cells with no clonality. No morphological and immune-phenotypic evidence of plasma cell dyscrasia was found, but BM biopsy did show numerous non-caseating granulomas consistent with sarcoidosis. Skin biopsy from non-scaly 6-mm skin colored papule also showed non-caseating granulomas. The patient had elevated angiotensin-converting enzyme levels (165 ug/l) and an erythrocyte sedimentation rate of 27 mm/h. Kidney biopsy did not show granulomas. The hypercalcemia, proteinuria, and AKI responded well after 2 weeks of 60 mg oral prednisone daily.

Acute lymphoblastic leukemia complicated by acute renal failure: a case report and review of the literature.

The patient, a previously healthy woman, presenting with acute renal failure and anemia, was admitted to our hospital. Her serum creatinine (Scr) had increased from 0.79 - 2.69 mg/dl over three days and hemoglobin had decreased from 12.1 - 7.8 g/dl over 4 weeks. Mild compression fracture and degeneration of the lumbar vertebra and skull were observed in X-ray. The renal biopsy showed acute proximal tubular lesions induced by multiple calcium deposition. A bone marrow biopsy showed that primitive lymphocyte was up to 92.5%. After making a diagnosis of acute lymphoblastic leukemia complicated with acute kidney injury induced by hypercalcemia, CRRT (continued renal replacement therapy) and chemotherapy were used immediately. Ten days later, the blood calcium had gradually decreased from 3.88 to normal range (1.8 mmol/l) and the renal function was back to normal (Scr 0.93 mg/dl). This unusual case shows that a patient who has a syndrome of acute renal failure, electrolyte disturbances, anemia, and elevated LDH needs bone marrow puncture to eliminate renal injury caused by hematologic diseases.

Hypophosphatemic rickets: A case of recurrent pathological fractures.

Renal phosphate-wasting disorders are the most common form of hereditary rickets and osteomalacia in western countries, but are rarely reported in India. Therefore, we report here a case of hypophosphatemic rickets. To report a case of hypophosphatemic rickets presenting with recurrent pathological fractures. A 34-year-old premenopausal lady presented with recurrent pathological fractures, bone pain, and muscle weakness since 14 years of age. A thorough history was taken followed by clinical examination, and relevant biochemical and radiological investigations were done. Height was 125 cm, arm span 145 cm, body weight 30 kg, and body mass index (BMI) 19.2 kg/m(2). Dental caries, kyphoscoliosis, shortening of left lower limb, bilateral coxa vara deformity of knee, muscle weakness, and bone tenderness were present. Calcium was 9.4 mg/dL, phosphorus: 1.8 mg/dL, albumin: 4.0 gm/dL, alkaline phosphatase: 360 U/L, creatinine: 0.4 mg/dL, a normal ammonium chloride (NH4Cl) loading test,24-hour urine calcium excretion: 102 mg/day, 25-hydroxyvitamin D3 [25(OH)D3]: 21.6 ng/mL, intact parathyroid hormone (PTH): 43.74 pg/mL, fraction excretion of phosphate (PO4): 40%, tubular maximum reabsorption of phosphate per unit of glomerular filtrate (TmP/GFR): 0.65 mg/dL, and fibroblast growth factor (FGF)23: 321.4 RU/mL. Skeletal X-rays showed multiple old fractures and pseudofractures. Magnetic resonance imaging (MRI) of the whole body showed no evidence of tumor. Fludeoxyglucose ((18)F)-positron emission tomography (FDG-PET) computed tomography (CT) scan revealed metabolically active marrow with multiple areas of fracture and FDG-avid lesions in both lungs but no CT-based findings. Hypophosphatemic rickets or osteomalacia, possibly hereditary, is a rare cause of recurrent pathological fractures.

Myeloma protein

Serum free light-chain measurement can detect free light chains in the blood. Monoclonal free light chains in the serum or urine are called Bence Jones proteins. Interpretation upon detection Blood serum paraprotein levels of more than 30 g/l is diagnostic of smouldering myeloma, an intermediate in a spectrum of step-wise progressive diseases termed plasma cell dyscrasias. Elevated paraprotein level (above 30 g/l) in conjunction with end organ damage (elevated calcium, kidney failure, anemia, or bone lesions) or other biomarkers of malignancy, is diagnostic of multiple myeloma, according to the diagnostic criteria of the International Myeloma Working Group, which were updated in 2014. Detection of paraprotein in serum of less than 30 g/l is classified as monoclonal gammopathy of undetermined significance in cases where clonal plasma cells constitute less than 10% on bone marrow biopsy and there is no myeloma-related organ or tissue impairment.

[Primary macroglobulinemia with hypercalcemia, renal failure and systemic amyloidosis].

This report deals with an unusual case of primary macroglobulinemia with hypercalcemia, chronic renal failure and systemic amyloidosis. In May 1990, a 63-year-old male was transferred to our hospital because of hypercalcemia (13.5 mg/dl) and renal failure. Clinical examinations showed anemia, macroglossia, lymph node swellings and hepatomegaly. Laboratory findings included Bence-Jones (kappa type) proteinuria (0.8 g/day), a monoclonal gammopathy of the IgM-kappa type (2.8 g/dl), a proliferation of lymphoid cells in the peripheral blood (5%) and the bone marrow (59.6%), and lymphomatous involvement of an inguinal lymph node. Serum creatinine concentration was 8.5 mg/dl. The serum levels of parathormone and vitamin D3 metabolites were normal. The roentgenogram of bones showed a compression fracture of the lumbar spine and systemic osteoporosis. The treatment included eel calcitonin, prednisolone and the CHOP regimen, followed by hemodialysis and plasmapheresis. The serum level of IgM increased to 4.6 g/dl. The patient died three months later and postmortem examination demonstrated marked systemic amyloidosis.

Management The protein electrophoresis test should be repeated annually, and if there is any concern for a rise in the level of monoclonal protein, then prompt referral to a hematologist is required. The hematologist, when first evaluating a case of MGUS, will usually perform a skeletal survey (X-rays of the proximal skeleton), check the blood for hypercalcemia and deterioration in renal function, check the urine for Bence Jones protein and perform a bone marrow biopsy. If none of these tests are abnormal, a patient with MGUS is followed up once every 6 months to a year with a blood test (serum protein electrophoresis). Although patients with MGUS have sometimes been reported to suffer from peripheral neuropathy, a debilitating condition which causes bizarre sensory problems to painful sensory problems, no treatment is indicated.

Primary hyperparathyroidism

Operative intervention can be delayed in patients over 50 years of age who are asymptomatic or minimally symptomatic and who have serum calcium concentrations <1.0 mg/dL (0.2 mmol/L) above the upper limit of normal, and in patients who are medically unfit for surgery More recently, three randomized controlled trials have studied the role of surgery in patients with asymptomatic hyperparathyroidism. The largest study reported that surgery resulted in an increase in bone mass, but no improvement in quality of life after one to two years among patients in the following groups: Untreated, asymptomatic primary hyperparathyroidism Serum calcium between 2.60–2.85 mmol/liter (10.4–11.4 mg/dl) Age between 50 and 80 yr No medications interfering with Ca metabolism No hyperparathyroid bone disease No previous operation in the neck Creatinine level < 130 μmol/liter (<1.47 mg/dl) Two other trials reported improvements in bone density and some improvement in quality of life with surgery.

[Infectious pleurisy as first sign of multiple myeloma in a young 28 years old].

Multiple myeloma is a malignant proliferation of plasma cells, mainly affecting the bone marrow. It rarely occurs in young patients. The medical observation study reveals multiple myeloma discovered through a purulent pleurisy in a 28-year-old subject. This patient was admitted to the pneumology service of the Mohamed V military hospital in Rabat for a fever and dyspnea evolving into a context of poor general condition. Clinical examination found a right pleural fluid effusion syndrome. The pleural puncture reveals a germ-free exudative purulent fluid without plasma cells. The myeloma diagnosis was suspected due to the combination of an aplastic normochromic normocytic anemia at 4.5g/dL of hemoglobin, an accelerated erythrocyte sedimentation rate, hypercalcemia, renal failure and osteolytic lesions located mainly in the skull and pelvis area, oriented by electrophoresis and serum protein immunosubstraction revealing a narrow peak in monoclonal beta-2 globulin at 70.56g/L with a lambda monoclonal gammopathy with immunoglobulin G, and confirmed by the myelogram showing a 74% rate of bone marrow plasma cells. The occurrence of myeloma at a young age is rare and the purulent pleurisy without plasma cells is a rare form of presentation and represents a poor prognosis.

Surgery_Schwartz

(RANKL) in the bone marrow. RANKL induces osteoclast differentiation and acti-vation. Myeloma cells inhibit osteoblast differentiation and activity. Serum and urine electrophoresis detect the M protein. Workup also includes complete blood cell count, erythrocyte sedimentation rate, calcium levels, renal function assessment, β2-microglobulin levels, and a skeletal survey. X-ray will show multiple punched out lytic lesions. Bone scans may be cold in about 30% of cases. The SPEP, UPEP, and bone marrow biopsy are helpful in diagnosis. Histology will show atypical plasma cells with eccentric nuclei, its appearance resembles a “signet ring (Fig. 43-49).” Plasmacytoma is a solitary tumor with a negative bone marrow biopsy, usually treated with radiation to the lesion. Myeloma is treated with bisphosphonates, chemo-therapy, stem cell transplantation, and radiation therapy. Surgi-cal stabilization and irradiation is done for pathologic fractures or impending fractures. Many patients with

Multiple myeloma

Asymptomatic/smoldering myeloma: Serum M protein >30 g/l (3 g/dl) or Clonal plasma cells >10% on bone marrow biopsy and No myeloma-related organ or tissue impairment Monoclonal gammopathy of undetermined significance (MGUS): Serum paraprotein <30 g/l (3 g/dl) and Clonal plasma cells <10% on bone marrow biopsy and No myeloma-related organ or tissue impairment or a related B-cell lymphoproliferative disorder Related conditions include solitary plasmacytoma (a single tumor of plasma cells, typically treated with irradiation), plasma cell dyscrasia (where only the antibodies produce symptoms, e.g., AL amyloidosis), and peripheral neuropathy, organomegaly, endocrinopathy, monoclonal plasma cell disorder, and skin changes.

[Laboratory diagnostic and prognostic factors: Multiple myeloma in Morocco].

ObjectivesThe purpose of this retrospective study was to clarify the factors for a laboratory diagnosis of multiple myeloma (Kahler's disease) and assess their prognostic value.MethodsThe study of all 10 patients with multiple myeloma seen during 2009 in the department of internal medicine and the haematology laboratory of HASSAN II University Hospital Centre in Fez. Work-ups for all patients included hemograms, sedimentation speed, electrophoresis of serum and urinary proteins, myelograms, creatinemia, calcemia, ß2-microglobulin, LDH and CRP.ResultsIn this series, the average age of the patients was 59 years and the sex ratio 1.3 (men). The laboratory tests showed anemia below 12 g/dl in 80% of the cases, with IgG accounting for 50% of the cases. The median concentration of the monoclonal component was 28 g/l. The prognostic assessments showed an increase in ß2-microglobulins and creatinemia in one case. CRP was elevated in all patients.ConclusionThe results from this study are consistent with those from other series. Protein electrophoresis and myelography results are major diagnostic elements, because they make it possible to rule out a monoclonal gammopathy of undetermined significance, for which treatment differs completely from that for multiple myeloma. ß2-microglobulin and CRP are independent prognostic factors providing important information about survival.

Rare case of non-producer variant of plasma cell dyscrasias with circulating plasma cells.

Non-producing variant of plasma cell disorders with circulating plasma cells is an aggressive variant of plasma cell dyscrasias with relatively poor outcomes. A 75-year-old man was admitted due to anaemia (90 g/L) and thrombocytopenia (9×10<sup9</sup/L). Comprehensive metabolic panel showed creatinine of 1.34 mg/dL, total protein of 6 g/dL, and corrected calcium was normal. Peripheral smear review showed 8% circulating atypical plasmacytoid cells. Bone marrow biopsy (BMB) confirmed plasma cell myeloma involving 90%-95% of bone marrow cellularity. Serum protein electrophoresis showed no monoclonal protein. Due to aggressive biology of non-producer variant and outcomes based on circulating plasma cells, he was started on VD-PACE (bortezomib, dexamethasone, cisplatin, doxorubicin, cyclophosphamide and etoposide) chemotherapy. BMB after cycle 1 chemotherapy showed no morphologic, immunophenotypic, or flow cytometric features of a plasma cell neoplasm. Given excellent treatment response cycle 2 was changed to VRD (bortezomib, lenalidomide and dexamethasone). Following two cycles of VRD, he underwent autologous haematopoietic cell transplantation. Day 80 BMB suggested stringent complete response.

InternalMed_Harrison

chains are useful for detecting and characterizing M spikes, supplemented by immunoelectrophoresis, which is especially sensitive for identifying low concentrations of M components not detectable by protein electrophoresis. A 24-h urine specimen is necessary to quantitate Bence Jones protein excretion. Serum alkaline phosphatase is usually normal even with extensive bone involvement because of the absence of osteoblastic activity. It is also important to quantitate serum β2-microglobulin and albumin (see below).

Glomerular filtration rate

For creatinine in μmol/L: For creatinine in mg/dL: Creatinine levels in μmol/L can be converted to mg/dL by dividing them by 88.4. The 32788 number above is equal to 186×88.41.154. A more elaborate version of the MDRD equation also includes serum albumin and blood urea nitrogen (BUN) levels: where the creatinine and blood urea nitrogen concentrations are both in mg/dL. The albumin concentration is in g/dL. These MDRD equations are to be used only if the laboratory has NOT calibrated its serum creatinine measurements to isotope dilution mass spectrometry (IDMS). When IDMS-calibrated serum creatinine is used (which is about 6% lower), the above equations should be multiplied by 175/186 or by 0.94086. Since these formulae do not adjust for body size, results are given in units of mL/min per 1.73 m2, 1.73 m2 being the estimated body surface area of an adult with a mass of 63 kg and a height of 1.7m.

An atypical presentation of multiple myeloma in a young patient with pathological fracture.

We report a case of a 34-year-old male with a history of pulmonary tuberculosis and pathological fracture of shaft of long bone presented with symptoms of lower respiratory tract infection. The patient did not have any typical symptoms of multiple myeloma or hypercalcemia on presentation. Throughout his hospitalization, his serum globulin level was very high along with mild normocytic normochromic anemia and mild renal function derangement without apparent cause. Acute phase markers of inflammation, for example, erythrocyte sedimentation rate (ESR) were not elevated in this patient and there was no lytic lesion in bone radiographs. He was eventually diagnosed as a case of stage 3 multiple myeloma by immuno-fixation electrophoresis and bone marrow study. Multiple myeloma represents a pathology of diverse distribution and has varied unusual presenting symptoms. We consider it an underdiagnosed disease often missed especially in young because it is not considered by clinicians.

Acute pancreatitis

Alternative Ranson score Ranson's score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT) Interpretation If the score ≥ 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely Or Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality APACHE II score "Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 8 points predicts 11% to 18% mortality Hemorrhagic peritoneal fluid Obesity Indicators of organ failure Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min PO2 <60 mmHg Oliguria (<50 mL/h) or increasing BUN and creatinine Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>

Pathologic Fractures -- Evaluation

Laboratory analysis should include a complete blood count, comprehensive metabolic panel (with special attention to serum calcium and alkaline phosphatase), prothrombin/INR, activated partial thromboplastin, erythrocyte sedimentation rate, urinalysis, urinary protein electrophoresis, and serum protein electrophoresis. Disease-specific markers, including prostate-specific antigen (PSA) and carcinoembryonic antigen (CEA), etc., may also be considered. Laboratory abnormalities may exist secondary to malignancy and may elucidate the source of malignancy. For example, a urinalysis may provide some insight into the primary pathology. If hematuria is present, renal cell or uroepithelial carcinoma should be considered. If Bence-Jones proteins are present, multiple myeloma is likely the diagnosis. Pregnancy tests should also be obtained in women of child-bearing age prior to imaging.

Ranson criteria

Acute pancreatitis not secondary to gallstones At admission: Blood glucose > 11.11 mmol/L (> 200 mg/dL) Age > 55 years Serum LDH > 350 IU/L Serum AST > 250 IU/L WBC count > 16000 cells/mm3 Within 48 hours: Serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit decreased by > 10% Oxygen (hypoxemia with PaO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L Acute pancreatitis secondary to gallstones At admission: Glucose > 220 mg/dl Age > 70 years LDH > 400 IU/L AST > 250 IU/ 100 ml WBC count > 18000 cells/mm3 Within 48 hours: Serum calcium < 8 mg/dL Hematocrit decreased by > 10% Base deficit > 4 mEq/L BUN increased by > 2 mg/dL Sequestered fluid > 6L

Importance of serum albumin level in the preoperative tests conducted in elderly patients with hip fracture.

Preoperative testing is commonly performed in patients undergoing surgery for hip fractures. The purpose of this study was to determine the appropriate preoperative tests after implementation of the case-payment reimbursement system and clinical pathway. We analysed 242 patients admitted to a regional hospital for hip fracture. Preoperative comorbidities and laboratory test results were measured and evaluated for their association with the occurrence of postoperative adverse outcomes. Univariate analysis showed that abnormal chest X-ray, haemoglobin, albumin, and total protein were associated with concomitant pulmonary diseases. Abnormal electrocardiogram (ECG), Na, creatinine, and aspirate aminotransferase (AST) levels were associated with heart disease. On the base of the univariate analysis, the significant preoperative variables for increased postoperative complications at 30 days included abnormal chest X-ray (odds ratio, 4.45; 95% confidence interval (CI), 2.24-8.84), ECG (odds ratio, 3.95; 95% CI, 1.96-7.95), Hct (odds ratio, 2.22; 95% CI, 0.96-5.16), Hb (odds ratio, 2.68; 1.29-5.58), blood urine nitrogen (odds ratio, 2.69; 95% CI, 1.34-5.42), creatinine (odds ratio, 4.49; 2.31-8.75), albumin (odds ratio, 9.68; 95% CI, 3.16-29.65), and AST (odds ratio, 2.36; 95% CI, 1.12-4.98). After adjustment for age, sex, and comorbidities, the risk factors that improved the predictability of postoperative complications were found to be abnormal chest X-ray (odds ratio, 6.03; 95% CI, 1.84-19.82) and albumin level (odds ratio, 6.23; 95% CI, 1.90-20.42). Serum albumin level and preoperative chest X-rays should be included in the preoperative routine tests recommended for elderly patient with hip fracture.

Latent iron deficiency

Latent iron deficiency (LID), also called iron-deficient erythropoiesis, is a medical condition in which there is evidence of iron deficiency without anemia (normal hemoglobin level). It is important to assess this condition because individuals with latent iron deficiency may develop iron-deficiency anemia. Additionally, there is some evidence of a decrease in vitality and an increase in fatigue among individuals with LID. Diagnosis Diagnostic tests for latent iron deficiency LID complete blood count hemoglobin serum iron total iron binding capacity serum ferritin bone marrow examination (rarely) Note: Iron therapy must be suspended 48 hours beforehand to ensure valid test results. The normal range for hemoglobin is 13.8 to 17.2 grams per deciliter (g/dL) for men and 12.1 to 15.1 g/dL for women. Low hemoglobin indicates anemia but will be normal for LID.