Pneumonia in adult

Definition

·       Pneumonia is defined as inflammation of the lung parenchyma

·       The microorganisms gain entry into the lungs by:

• Inhalation
• Aspiration
• Haematogenous spread
• Direct spread
• Reactivation of latent infection

Classification and Epidemiology

·       Classification is based on various characteristics of the illness such as

• The setting or mechanism of acquisition
• Pathogen responsible/aetiology
• Anatomic or radiologic distribution

Classification Based on Setting or Mechanism of Acquisition of Infection

Community-acquired Pneumonia (CAP)

·       Defined as pneumonia that develops in the outpatient setting or within 48 hours of admission to a hospital.

·       The incidence varies with age, being much higher in the very young and the elderly.

·       Pneumonia accounts for almost one-fifth of childhood deaths world-wide, with approximately 2 million children under 5 dying each year

·       CAP is usually spread by droplet infection and most cases occur in previously healthy individuals.

·       Several factors can impair the effectiveness of local defences and predispose to pneumonia.

• Cigarette smoking
• Upper respiratory tract infections
• Alcohol
• Corticosteroid therapy
• Old age
• Recent influenza infection
• Pre-existing lung disease

·       Once the organism settles in the alveoli, an inflammatory response ensues. The classical pathological responses evolve through the phases of congestion, red and then grey hepatisation, and finally resolution with little or no scarring.

·       The majority of cases of CAP are due to infection with Strep. pneumoniae

·       Thereafter the most likely alternatives depend on the age of the patient and the clinical circumstances.

·       For example, Mycoplasma  pneumoniae and Chlamydia  pneumoniae are common in young adults but seldom reported in the elderly, whereas Haemophilus influenzae should be considered in elderly patients but is rarely reported in young adults.

Clinical Features

·       CAP typically presents as an acute illness in which systemic features such as fever, rigors, shivering and vomiting often predominate.

·       The appetite is usually lost and headache frequently reported.

·       Pulmonary symptoms include cough, which at first is characteristically short, painful and dry, but later accompanied by the expectoration of mucopurulent sputum.

·       Rust-coloured sputum may be seen in patients with Streptococcus pneumoniae, and the occasional patient may report haemoptysis.

·       Pleuritic chest pain may be a presenting feature and on occasion may be referred to the shoulder or anterior abdominal wall.

·       Upper abdominal tenderness is sometimes apparent in patients with lower lobe pneumonia or if there is associated hepatitis.

Hospital-Acquired Pneumonia

·       Hospital-acquired or nosocomial pneumonia refers to a new episode of pneumonia occurring at least 2 days after admission to hospital.

·       The term includes post-operative and certain forms of aspiration pneumonia, and pneumonia or bronchopneumonia developing in patients with chronic lung disease, general debility or those receiving assisted ventilation.

·       The factors predisposing to the development of pneumonia in a hospitalised patient are

• Reduced host defences against bacteria
• Reduced immune defences (e.g. corticosteroid treatment, diabetes, malignancy)
• Reduced cough reflex (e.g. post-operative)
• Disordered mucociliary clearance (e.g. anaesthetic agents)
• Bulbar or vocal cord palsy
• Aspiration of nasopharyngeal or gastric secretions

§  Immobility or reduced conscious level

§  Vomiting, dysphagia, achalasia or severe reflux

§  Nasogastric intubation

• Bacteria introduced into lower respiratory tract

§  Endotracheal intubation/tracheostomy

§  Infected ventilators/nebulisers/bronchoscopes

§  Dental or sinus infection

• Bacteraemia

§  Abdominal sepsis

§  Intravenous cannula infection

§  Infected emboli

Aetiology of Hospital Acquired Pneumonia

·       Majority of hospital-acquired infections are caused by Gram-negative bacteria.

·       These include Escherichia, Pseudomonas and Klebsiella species. Infections caused by Staphylococcus aureus (including multidrug-resistant-MRSA-forms) are also common in hospital, and anaerobic organisms are much more likely than in pneumonia acquired in the community.

·       Physiotherapy is of particular importance in the immobile and elderly, and adequate oxygen therapy, fluid support and monitoring are essential. The mortality from hospital-acquired pneumonia is high (approximately 30%).

Suppurative and Aspirational Pneumonia

·       Suppurative pneumonia is the term used to describe a form of pneumonic consolidation in which there is destruction of the lung parenchyma by the inflammatory process.

·       Suppurative pneumonia may be produced by infection of previously healthy lung tissue with Staphylococcus aureus or Klebsiella pneumoniae.

·       These are, in effect, primary bacterial pneumonias associated with pulmonary suppuration.

·        More frequently, suppurative pneumonia and pulmonary abscess develop after the inhalation of septic material during operations on the nose, mouth or throat under general anaesthesia, or of vomitus during anaesthesia or coma.

·        In such circumstances gross oral sepsis may be a predisposing factor.

·        Additional risk factors for aspiration pneumonia include bulbar or vocal cord palsy, achalasia or oesophageal reflux and alcoholism.

·       Aspiration into the lungs of acid gastric contents can give rise to a severe haemorrhagic pneumonia often complicated by the acute respiratory distress syndrome (ARDS).

·       Injection drug-users are at particular risk of developing haematogenous lung abscess.

·       Bacterial infection of a pulmonary infarct or of a collapsed lobe may also produce a suppurative pneumonia or a lung abscess.

·       The organism(s) isolated from the sputum include Strep pneumoniae, Staph. aureus, Strep. pyogenes, H. influenzae and, in some cases, anaerobic bacteria.

Clinical Features of Suppurative Pneumonia

·       Cough productive of large amounts of sputum which is sometimes fetid and blood-stained

·       Pleural pain common

·       Sudden expectoration of copious amounts of foul sputum occurs if abscess ruptures into a bronchus

·       High remittent pyrexia

·       Profound systemic upset

·       Digital clubbing may develop quickly (10-14 days)

·       Chest examination usually reveals signs of consolidation; signs of cavitation rarely found

·       Pleural rub common

·       Rapid deterioration in general health with marked weight loss can occur if disease not adequately treated.

Pneumonia in Immunocompromised Patient

·       Pulmonary infection is common in patients receiving immunosuppressive drugs and in those with diseases causing defects of cellular or humoral immune mechanisms.

·       It is important to appreciate that the majority of infections are caused by the same common pathogens that cause pneumonia in non-immunocompromised individuals

·       Gram-negative bacteria, especially Pseudomonas aeruginosa, are more of a problem than Gram-positive organisms, and unusual organisms or those normally considered to be of low virulence or non-pathogenic may become 'opportunistic' pathogens.  Importantly infection is often due to more than one organism.

Clinical Features

·       The patient usually presents with fever, cough, breathlessness and infiltrates on the chest X-ray.

·       Patients may develop non-specific symptoms.

  Refer to Handout 5.1: Pathophysiology and Classification of Pneumonia

Symptoms and Signs of Pneumonia

Symptoms

·       The presence of cough, particularly cough productive of sputum, is the most consistent presenting symptom.

·The character of the sputum may suggest a particular pathogen, as follows: 

• Rust-colored sputum  - frequently associated with infection by S pneumoniae
• Currant-jelly sputum  - frequently associated with infection by Klebsiella species
• Foul-smelling or bad-tasting sputum  - often produced by anaerobic infections

·       Chest pain

·       Dyspnea

·       Hemoptysis (when clearly delineated from hematemesis)

·       Decreased exercise tolerance

·       Abdominal pain from pleuritis is also highly indicative of a pulmonary process 

·       Nonspecific symptoms such as high grade fever, rigors or shaking chills, and malaise are common.

·       Other nonspecific symptoms that may be seen with pneumonia include myalgias, headache, nausea, vomiting, diarrhoea, and altered sensorium.

Signs

·       Hyperthermia (fever, typically >38°C) or hypothermia (<35°C)

·       Tachypnea (>18 respirations/min)

·       Use of accessory muscles of respiration

·       Tachycardia (>100 breaths per minute) or bradycardia (<60 beat per minute)

·       Central cyanosis

·       Altered mental status

Other Signs

·       Adventitious breath sounds, such as rales/crackles, rhonchi or wheezes and bronchial breathing sounds during consolidation stage decreased intensity of breath sounds

·       Egophony

·       Whispering pectoriloquy

·       Dullness to percussion

·       Lymphadenopathy

Differential Diagnosis, Investigations, Treatment and Complications of Pneumonia

Differential Diagnosis of Pneumonia

·       Pneumocystis jerovecii pneumonia (Formally called Pneumocystis carinii pneumonia)

·       Chronic obstructive pulmonary disease (COPD)

·       Bronchiectasis

·       Chronic bronchitis

·       Foreign body aspiration

·       Influenza

·       Lung abscess

Investigation

·       Sputum

• Gram- or Ziehl-Neelsen staining
• Culture and sensitivity (this can be done at hospital level)

·       Chest x-ray (only at hospital level)

• In Lobar pneumonia the findings are Homogeneous opacity localized to the affected lobe or segment. This is usually appears within 12-18 hours of the onset of illness.
• In bronchopneumonia the findings: Patchy alveolar consolidation

·       Blood (mostly at hospital level)

• Culture and sensitivity- hospital level
• Full blood picture

§  Neutrophilia favours the diagnosis of bacterial pneumonia, particularly pneumococcal pneumonia

Treatment

·       Oxygen therapy or Mechanical ventilation-depending on severity. This requires referral of the patient to hospital because oxygen therapy is not readily available in primary health care facilities

·       Intravenous fluid

• Most patients with moderate to severe pneumonia also require intravenous fluids and occasionally inotropic support.

·       Analgesics

• They are important to allow the patient to breathe normally and cough efficiently e.g.   Paracetamol

·       Antibiotics

A: Uncomplicated Community Acquired Pneumonia

·       Duration of treatment: 7-10 days are adequate, although treatment may require 14 days or more in patients with Legionella, staphylococcal or Klebsiella pneumonia.

·       Amoxicillin 500 mg 8 hourly orally

    If patient is allergic to penicillin

·       Clarithromycin 500 mg 12 hourly orally.  Or Erythromycin or Tetracycline 500 mg 6 hourly orally

B: Severe Community Acquired Pneumonia

·       The patient needs to be admitted in intensive care unit (at hospital level).

·       Ampicillin IV or Benzyl penicillin IM  plus Chloramphenicol or

·       Ceftriaxone 1-2 g daily IV with

·       Supportive care e.g. monitor vital signs, Oxygen therapy, analgesics, bed rest, IV fluids

Suppurative Pneumonia

·       Ampicillin IV 6 hourly or IM Benzyl penicillin then followed by oral Amoxicillin.

·       If an anaerobic bacterial infection is suspected (e.g. from fetor of the sputum), oral Metronidazole 400 mg 8-hourly should be added sputum.

·       Prolonged treatment for 4-6 weeks may be required in some patients with lung abscess.

·       Removal or treatment of any obstructing endobronchial lesion is essential.

Complications

·       Lung abscesses

·       Development of bacteremia with metastatic abscess in other organs to cause (Meningitis, Endocarditis, Arthritis, Pericarditis, Hepatitis)

·       Spread to pleural cavities producing empyema

·       Spread to pericardial cavity leading to suppurative pericarditis

·       Consolidation of the lung parenchyma

·       Para Pneumonic effusion presenting as Pleural effusion

·       Retention of sputum causing lobar collapse

·       Pyrexia due to drug hypersensitivity

Prognosis

Features associated with a high mortality in pneumonia are as outlined below

·       Clinical parameters

• Age: ≥60 years
• Respiratory rate: > 30 cycles/min
• Diastolic blood pressure: <60 mmHg
• Confusion
• More than one lobe involved on chest x-ray
• Presence of underlying disease

·       Therefore, all patients who are thought of having severe form of pneumonia should be referred to hospital for proper diagnosis and treatment.

Asthma Morbidity and Treatment in Children With Sickle Cell Disease

Abstract and Introduction

Abstract

Children with sickle cell disease (SCD) and a comorbid condition of asthma have increased numbers of vaso-occlusive pain and acute chest syndrome episodes, and all-cause mortality. When assessed systematically, asthma prevalence is probably similar among children with SCD when compared with the general African–American population. With increasing recognition of the importance of asthma in the management of SCD, hematologists must become familiar with asthma and develop a multidisciplinary approach, including early recognition, appropriate management and referral to asthma specialists.

Introduction

Sickle cell disease (SCD) is one of the common hemoglobinopathies worldwide and is inherited as an autosomal recessive disorder by mendalian genetics. Hemoglobin SS (SCD-SS) and sickle cell-β⁰thalassemia (SCD-S β⁰thal) are the most severe phenotypes, occurring in approximately 60% of individuals with SCD in North America. Other compound heterozygote phenotypes, including hemoglobin SC (SCD-SC) and sickle cell-β+ thalassemia (SCD-Sβ+ thal) occur in approximately 9–12% and 1%, respectively, based on data from newborn cohort studies. The underlying defect in SCD-SS is a single nucleotide substitution, which results in a hemoglobin molecule that has substitution of glutamic acid with valine at position 6 of the β-globin molecule. SCD-SC occurs from single nucleotide exchange resulting in the substitution of glutamic acid with lysine also at position 6 of the hemoglobin molecule. These amino acid switches change the net electrical charge of the hemoglobin molecule making it easily susceptible to polymerization under states of low oxygen tension and stress. SCD-Sβ+ thal and SCD-Sβ⁰thal phenotypes are due to impaired production of β-hemoglobin chains resulting from gene deletions or mutations in the presence of the sickle cell mutation in the other β-globin allele. SCD-Sβ+ thal is characterized by decreased production, and SCD-Sβ⁰thal by complete absence, of the β-chain. Atopic asthma, a chronic disorder of the airways, is characterized by recurrent episodes of airway narrowing from inflammation, mucus plugging and bronchoconstriction culminating in airway remodeling. Similar to SCD, asthma exhibits significant heterogeneity in clinical presentation in children. Diagnosis of asthma is primarily based on symptoms and clinical findings, and can be supported by pulmonary function tests, such as the presence of airway obstruction and bronchodilator response on spirometry, which may also be useful in monitoring effectiveness of treatment. Supporting laboratory tests include elevation of total serum IgE levels, peripheral blood eosinophilia and specific allergen sensitivity. Despite being supportive for the diagnosis of asthma, the use of laboratory or pulmonary function studies alone are not indicative of an asthma diagnosis. In our clinical experience, in the setting of acute asthma exacerbation, many patients with SCD will not have decreased oxygen saturation^[10] and will not have any audible wheezing; however, when spirometry is performed there is evidence of airway reversibility that correlates with the current symptoms.

Epidemiology of Asthma & SCD

Newborn screening data between 1990 and 1999 reported an incidence of SCD of one in 2474 of live births.^[11] All 50 states and the District of Colombia currently have active screening programmes for hemoglobinopathies.^[12] In the USA, SCD population estimates ranged from 104,000 to 138,900 based on birth cohort disease prevalence, but from 72,000 to 98,000 when corrected for early mortality.^[13]

The past 20 years have seen a doubling in the incidence of asthma, with about 34 million people affected.^[14] Between 2006 and 2008, asthma prevalence was 9.3% amongst children under the age of 17 years, with prevalence in African–Americans at 14.6% and multiracial children, 13.6%, when compared with Caucasians, 8.2%.^[15] Unlike children, the prevalence of asthma in African–Americans adults is 7.8%, similar to the general population prevalence of 7.3%.^[15] These prevalence estimates for asthma were based on eliciting a positive response by an adult member of a family to the question 'have you ever been told by a doctor or other health care professional that you have asthma?' and 'do you still have asthma?'.^[15] When the prevalence of asthma in SCD is compared with the general African–American population, there appears to be a similar or slightly higher prevalence of asthma, only one study was designed to address prevalence in the same geographic area (Table 1). Variation in asthma prevalence in SCD is as a result of different definitions used in the diagnosis of asthma. Less stringent definitions of asthma as well as a selection bias towards individuals with underlying lung disease results in a higher prevalence of asthma. However, in Saint Louis (MO, USA) where children with SCD have been assessed for asthma using standardized clinical and pulmonary function criteria, the prevalence of asthma in SCD is similar to that seen in the Saint Louis city elementary schools where the racial mixture is similar to that in the SCD clinic.

Rationale for Article

Asthma is a distinct, common comorbid condition in SCD; associated with an increase in SCD-related morbidity and premature mortality. Despite the well recognized clinical entity of asthma, particularly in children, nuances of asthma diagnosis in children with SCD are challenging with common symptoms of asthma such as cough, wheeze, chest pain and exercise intolerance attributed to infection or SCD instead of asthma. Further compounding the diagnosis is the fact that while positive test results for airway lability, such as methacholine challenge test and bronchodilator response, are strong predictors for asthma in the general population, their association with asthma in SCD is far less clear. In children with SCD, a physician diagnosis of asthma remains the primary basis of children at risk for pain and acute chest syndrome. Among all children with SCD, evaluation for asthma risk factors should be carried out routinely and repeatedly, but the results of these tests should not supersede the physician diagnosis of asthma. Understanding the nuances of diagnosis of asthma, particularly in children with SCD, is critical because a physician diagnosis of asthma is one of the few established risk factors associated with SCD-related morbidity.

Optimal management of asthma in children with SCD has not been established, but practical approaches to care can be gleaned from asthma management in the general population. Until more asthma specific studies on therapy in SCD are available, asthma in children and adults with SCD should be recognized early and managed according to National Heart, Lung and Blood Institute (NHLBI) guidelines for asthma therapy in the general population. This article will highlight challenges in diagnosis and management of asthma among individuals with SCD.

Asthma & Sickle Cell Pain

Vaso-occlusive pain is the leading cause of admissions to hospital, and even in a state of relative good health, a significant number of children have some amount of pain. In the multi-institutional study, Cooperative Study of Sickle Cell Disease (CSSCD), a prospective cohort of 291 infants was followed for a mean length of 11 years and 4062-patient-years. Of these children, 16.8% had a diagnosis of asthma. An increased incidence of painful episodes (1.39 vs 0.47 events per patient-year; p < 0.001) was noted in children with asthma compared with those without asthma. In a second cohort study of 1016 children from the Silent Cerebral Infarct Multi-Center Clinical (SIT) trial, a diagnosis of asthma occurred in 22% of the cohort and was associated with an increased rate of vaso-occlusive pain episodes that resulted in hospitalization and acute chest syndrome (ACS) episodes. After final adjustment for age, hemoglobin F and baseline hemoglobin levels, vaso-occlusive pain rates were 73 and 57 episodes per 100 patient-years among children with and without an asthma diagnosis respectively (p = 0.0176). However, a single institution retrospective cohort study from France did not find an impact of asthma on pain episodes. A total of 297 children with sickle cell anemia were enrolled, 25 with a history of asthma and 272 without a history of asthma, with follow-up at 7 and 6 years, respectively, for a total of 1805 patient-years. No association existed between asthma and the rate of vaso-occlusive pain episodes (72 and 60 pain episodes per 100 patient-years; p = 0.53). This lack of association between asthma and SCD-related pain might be attributed to: the sample size, as the absolute rate of pain for patients with and without asthma were similar to that obtained in the CSSCD; differences in management of pain within France;^[21] or the inherent limitations of a single-center study when compared with a multicentered study that did find a significant relationship between vaso-occlusive pain and asthma.

Lower airway obstruction (LAO) is a common risk indicator of asthma. Using spirometry in a single institutional study with LAO defined as forced expiratory volume in 1 s (FEV₁)/forced vital capacity ratio (FVC) < 95% CI and adjusted for age and gender,^[22] children with LAO had more than twofold the admission rates for either pain or ACS compared with children with normal lung function when assessed prospectively from time of pulmonary function test (PFT).^[23] In this review of PFT records of 102 children with SCD, children with LAO had twice the rate of morbidity when compared with children with normal lung function (2.5 vs 1.2 hospitalizations for pain or ACS per patient-year; p = 0.003; risk ratio: 2.0; 95% CI: 1.3–3.3). Children with restriction did not have different rates of future morbidity compared with children with normal lung function (1.4 vs 1.2 hospitalizations for pain or ACS per patient-year; p = 0.68; rate ratio: 1.1; 95% CI: 0.6–2.1). LAO was also associated with increased risk of morbidity, even in those children without a diagnosis of asthma. Several limitations exist in this study, including but not limited to referral bias of a hospital based cohort that had to receive spirometry evaluation for inclusion and a small sample size that is sensitive to outliers. As a single institution study with several limitations, the study results require repeating before significant confidence can be placed in the association between LAO- and SCD-related morbidity.

Asthma & Acute Chest Syndrome

Acute chest syndrome is the leading cause of death and admissions to the pediatric intensive care unit in children and adolescents, and the second most common cause of admission after vaso-occlusive pain episodes in children. Multiple ACS definitions have been proposed; although significant differences exist in terms of clinical symptoms needed, it is accepted that an infiltrate or new radiodensity on imaging is an important criterion that needs to be fulfilled. Other clinical features include hypoxemia, respiratory distress, fever, need for blood transfusion and rapid deterioration in clinical status. Differentiating between an acute asthma exacerbation and ACS is a challenge clinically as they can present with similar symptoms. Wheezing and cough, a common clinical presentation of asthma, are also common findings of ACS, and a new radiodensity on chest x-ray may represent either atelectasis or infiltrate. One usually needs to treat for both asthma and ACS in the setting of a previous doctor diagnosis of asthma. In the CSSCD infant cohort, asthma was associated with more frequent ACS episodes, 0.39 versus 0.20 events per patient-year (p < 0.001),^[18] and a similar twofold rate of ACS per patient-year (0.31 vs 0.16 events/patient; p = 0.03) was found in the French study.^[21] Recurrent ACS episodes are associated with abnormal lung function among children with SCD.^[27] Also, the proportion of children with a physician diagnosis of asthma increases linearly as the number of ACS episodes increase.^[28]

Given, the intrinsic limitations of the study design of most SCD studies, where careful delineation of asthma was not part of the original purpose of the study, we are unable to determine whether ACS predisposes to asthma or vice versa. However, children with ACS are diagnosed with asthma at a younger age compared with those without ACS,^[29] suggesting that asthma is a predictor of the occurrence of ACS. In the SIT trial, involving 1016 children with SCD, An et al. also confirmed that a doctor diagnosis of asthma was associated with increased incidence rates of ACS.^[19] In this large study, after final adjustment for age, hemoglobin F and baseline hemoglobin levels, ACS incidence rates were 22 and 12 episodes per 100 patient-years among children with and without an asthma diagnosis, respectively (p < 0.0001). Severe recurrent wheezing is associated with increased rates of hospitalization for ACS, risk ratio = 2 (95% CI: 1.2–3.4; p = 0.005). In a retrospective study, by Knight-Maddenet al. children with recurrent episodes of ACS were more likely to have atopic asthma and bronchial hyper-reactivity compared with those with only a single ACS event, 53 versus 8% (Odds ratio [OR]: 8.1; 95% CI: 2.3–28.6; p < 0.001). While the results of these studies do not demonstrate causality, they show a close association between ACS and asthma, suggesting that a diagnosis of asthma predisposes to future ACS episodes.

The diagnosis of asthma at different ages is a challenge particularly in younger children; our group follows the premise that asthma is a lifelong condition, as demonstrated by progressive decline in lung function over 15 years in persons who gave a self report of asthma and at 28 years in children with frequent wheezing. Probably the most compelling support that a diagnosis of asthma precedes ACS is based on the observation that in the CSSCD, children with a diagnosis of asthma presented with ACS at 2.4 years compared with 4.6 years in children without asthma (hazard ratio: 1.64; 95% CI: 1.13–2.39; p = 0.01). Additionally, results from two retrospective studies, suggest, but do not confirm, that a previous diagnosis of asthma is associated with future ACS episodes. In the first study a history of asthma and home use of inhaled β adrenergic agonists were associated with increased readmission within 14 days of discharge for an ACS episode, OR = 3.8 (95% CI: 0.9–15; p = 0.06) and OR = 6 (95% CI: 1.2–3; p < 0.05), respectively. In the second study, Boyd et al. reviewed medical records of children admitted for pain of children with asthma (cases), 35% developed ACS in hospital compared with 12% in children without asthma (controls). Children with a physician diagnosis of asthma were about four-times more likely to develop ACS and also had longer hospitalizations for ACS, 5.6 compared with 2.6 days (p = 0.01). The association between asthma and SCD is not limited to patients with hemoglobin SS. In a retrospective study, a greater proportion of children with SCD-SC had a prior history of asthma or wheezing than those with SCD-SS, 50.7 versus 33.8% (p = 0.04).

Asthma & Mortality

Life expectancy in SCD has improved over the past 20–30 years and is partially dependent on SCD phenotype. In a prospective study that followed 3764 individuals from birth to 66 years of age, the median age at death for males and females were 42 and 48 years of age for SCD-SS and SCD-Sβ⁰thal, but 60 and 68 years of age for SCD-SC, respectively (p < 0.001), much lower than the general population. Pulmonary findings on autopsy may include findings consistent with acute asthma exacerbation and or pulmonary hypertension.

A risk for premature death among those with SCD-SS and asthma was demonstrated in the CSSCD prospective cohort of 138 individuals with asthma and 1825 individuals without asthma. Individuals were identified at a mean age of 9.7 and 14.2 years (p < 0.001), respectively, and followed for a total of 18,495 patient-years. Hazard ratio for the comorbid condition of asthma was 2.36 (95% CI: 1.21–4.62; p = 0.01). Although result of this study does not establish a cause and effect relationship between asthma and premature mortality, it provides compelling support of at least a strong association.

A causal link between the presence of asthma and premature death is suggested by the report of Field et al. of two adolescents with histories of severe persistent asthma in addition to SCD Both individuals were prescribed appropriate treatment for their asthma and had recently received medical care from a pediatric asthma specialist; however, both adolescents died suddenly in the midst of increased respiratory symptoms consistent with asthma exacerbation, where post mortem findings were consistent with asthma. Taken together, these data underscore the importance of not only diagnosing asthma in children and adults with SCD, but also understanding the optimal management for this vulnerable population.

Assessment of sick child

To assess a sick child, one have to check on various things, emergency signs and priority signs

Emergency signs

For emergency signs, following have to be checked since they can cause death at any time, immediate action should be taken in case emergency signs are seen.

·        Obstructed breathing

·        Severe respiratory distress

·        Central cyanosis

·        Signs of shock(weak pulse, slow capillary refill, cold extremities)

·        Coma

·        Convulsion

·        Signs of severe dehydration(sunken eyes, skin pinch return slowly)

If there are no emergency signs, assess for priority signs, the priority signs are

·        Trauma(injury)

·        Temperature(fever)

·        Tiny baby

·        Pallor

·        Pain

·        Poisoning

·        Restless

·        Respiratory distress

·        Referral

opening cotc lindi

beric,
the officials at clinical officer training college lindi urges students at clinical officer training center to return to the college on 28th april. the date above has been set by principle dr mnyani who personaly said that there has been two weeks addition in previous holiday so he will not expect any excuse.
whoever read this should inform others

a doctor who planted doctrine seeds in my heart

Benjamin Solomon "Ben" Carson, Sr., M.D., (born September 18, 1951) is an American neurosurgeon and the Director of Pediatric Neurosurgery at Johns Hopkins Hospital. He was awarded the Presidential Medal of Freedom, the highest civilian award in the United States, by President George W. Bush in 2008.

Carson was born in Detroit, Michigan and was raised by his single mother, Sonya Carson. He struggled academically throughout elementary school, but started to excel in middle school and throughout high school. After graduating with honors from his high school, he attended Yale University, where he earned a degree in Psychology. He chose to go to Yale because in College Bowl, an old TV program, he saw Yale compete against and defeat many other colleges in knowledge, including Harvard. Carson wanted to participate in College Bowl, but the program was discontinued. From Yale, he attended University of Michigan Medical School.

ben curson, a mentor in my life and comming carier

Career

Carson's eye-hand coordination and three-dimensional reasoning skills made him a gifted surgeon.[1] After medical school he became a neurosurgery resident at Johns Hopkins Hospital in Baltimore. Starting off as an adult neurosurgeon Carson became more interested in pediatrics. With children he believed that "what you see is what you get,[2] ... when they’re in pain they clearly show it with a frown on their face or when they are happy they show it by smiling brightly." Since then he has been the head of the pediatric neurosurgeon department.[3]

At age 33, he became the hospital's youngest major division director, as Director of Pediatric Neurosurgery. Carson's other surgical innovations have included the first intrauterine procedure to relieve pressure on the brain of a hydrocephalic fetal twin, and a hemispherectomy, in which a young girl suffering from uncontrollable seizures had one half of her brain removed.

In 1987, Carson made medical history by being the first surgeon to successfully separate siamese twins (the Binder twins) conjoined at the back of the head (craniopagus twins). The 70-member surgical team, led by Carson, worked for 22 hours. At the end, the twins were successfully separated and can now survive independently. Carson recalls:
I looked at that situation. I said, ‘Why is it that this is such a disaster?’ and it was because they would always exsanguinate. They would bleed to death, and I said, ‘There's got to be a way around that. These are modern times.’ This was back in 1987. I was talking to a friend of mine, who was a cardiothoracic surgeon, who was the chief of the division, and I said, ‘You guys operate on the heart in babies, how do you keep them from exsanguinating’ and he says, ‘Well, we put them in hypothermic arrest.’ I said, ‘Is there any reason that -- if we were doing a set of Siamese twins that were joined at the head -- that we couldn't put them into hypothermic arrest, at the appropriate time, when we're likely to lose a lot of blood?’ and he said, ‘No way .’ I said, ‘Wow, this is great.’ Then I said, ‘Why am I putting my time into this? I'm not going to see any Siamese twins.’ So I kind of forgot about it, and lo and behold, two months later, along came these doctors from Germany, presenting this case of Siamese twins. And, I was asked for my opinion, and I then began to explain the techniques that should be used, and how we would incorporate hypothermic arrest, and everybody said ‘Wow! That sounds like it might work.’ And, my colleagues and I, a few of us went over to Germany. We looked at the twins. We actually put in scalp expanders, and five months later we brought them over and did the operation, and lo and behold, it worked.[4]

Awards and honors

Carson has received numerous honors and many awards over the years, including over 61 honorary doctorate degrees. He was also a member of the American Academy of Achievement, the Horatio Alger Association of Distinguished Americans, the Alpha Omega Alpha Honor Medical Society, the Yale Corporation (the governing body of Yale University), and other prestigious organizations. He sits on many boards including the Board of Directors of Kellogg Company, Costco Wholesale Corporation, and America's Promise. He was also the president and co-founder of the Carson Scholars Fund, which recognizes young people of all backgrounds for exceptional academic and humanitarian accomplishments. In 2007, Carson was inducted into the Indiana Wesleyan University Society of World Changers and received an honorary doctorate while speaking at the university. He returned to IWU the following year when his friend, Tony Dungy, was also inducted into the society.[5] On June 19, 2008, Carson received the Presidential Medal of Freedom from President George W. Bush. He is a recipient of the Ford's Theatre Lincoln Medal and the William E. Simon Prize for Philanthropic Leadership, and was elected to the Institute of Medicine (IOM) of the United States National Academy of Science.
Publications and appearances

Carson has written four bestselling books published by Zondervan, an international Christian media and publishing company: Gifted Hands, The Big Picture, Take the Risk, and Think Big. The first book is an autobiography and two are about his personal philosophies of success that incorporate hard work and a faith in God; Carson is a Seventh-day Adventist. In a debate with Richard Dawkins, Francis Collins, and Daniel Dennett, Carson stated he doesn't believe in evolution: "I don't believe in evolution...He says that because there are these similarities, even though we can't specifically connect them, it proves that this is what happened.

Personal life

In June 2002 Carson was forced to cut back on his public appearances when he was diagnosed with prostate cancer, but the cancer was caught in time. He still operates on more than 300 children a year, but has been trying to shorten his days: prior to his cancer he used to work from 7:00 in the morning until 8:00 at night.

Carson married Candy Rustin, whom he met at Yale in 1975; she holds a M.B.A. degree and is an accomplished musician, and both are members of the Seventh-day Adventist Church.

Publications Wikiquote has a collection of quotations related to: Ben Carson

(2009) Gifted Hands: The Ben Carson Story,
(2008) Take The Risk,
(2000) The Big Picture,
(1996) Think Big, .

why clinical officer training center and not university

beric greyson aliila

good evening everyone who happen to read this article,
there is this question i ask myself, i reason with myself, and may be discus with myself, my answer will be quiet different from other people's point of view, even your view possibly. as any other student of tanzania who happen to have chance to go to a level, the only expectation in future is usually going to university. others probably knew nothing about clinical officer, i was among those students with same view and expectation.
it is quit easy from that point to conclude that diploma in medicine is a chance for failures. it is a very quick conclusion, and reasonable because it comes as the only option to some students.
as a young boy after finishing my ordinary level, my choice was to continue with physics, chemistry and biology while my dad thought i was more good in maths than biology. because it was my carrier, i did what i loved to do. when i completed a level, my dad strongly suggested that i apply for degree in education, i refused, and decided to apply for diploma in medicine. it was not the first time i head about diploma in medicine though, i knew about it when i was still studying a level.
a question that i ask myself every day and may be is a reason for me to be here today with strong will to complete this course, is because of what i want with  diploma in medicine. somewhere in my life as a member of college, i realized that nothing should really mater in ones life like his or her own future. i myself met challenges in emotional way and physical way and in the end every time i was depressed, the only thing that kept me going is why am i here.

i am not here so that i can be employed, i am here because i have dreams that depends on this, i came here because i was inspired by people, i am here because my life has nothing to live for but my dreams. to hold a phd in medicine, i realized that even though i earned division three in a level, it didnt mean that my dreams to be a doctor were dead, it was challenge, and coming here was one step to change the tide. i had love for my dream. i knew nobody was going to help me reach my goals, i had myself to depend on.
now think of yourself, why are you at clinical officer training centre?
is this your destination?
is this your dream?
if you lost the track, it is time to sit down and think again of your future.
beric