📖 General Pathology

Q Fever

An acute disease caused by Coxiella burnetii (Rickettsia burnetii) and characterized by sudden onset of fever, headache, malaise, and interstitial pneumonitis.

Symptoms and Signs

The incubation period varies from 9 to 28 days and averages 18 to 21 days. Onset is abrupt, with fever, severe headache, chills, severe malaise, myalgia, and, often, chest pains. Fever may rise to 40° C (104° F) and persist for 1 to > 3 wk. Unlike other rickettsial diseases, Q fever is not associated with a cutaneous exanthem. A nonproductive cough and x-ray evidence of pneumonitis often develop during the 2nd wk of illness.

In severe cases, lobar consolidation usually occurs, and the gross appearance of the lungs may resemble that of bacterial pneumonia

About 1/3 of patients with protracted Q fever develop hepatitis, characterized by fever, malaise, hepatomegaly with right upper abdominal pain, and possibly jaundice. Liver biopsy specimens show diffuse granulomatous changes, and C. burnetii may be identified by immunofluorescence.

EMBOLISM 

An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

99% due to dislodged thrombus

Types: 
1. Thrombo-embolism 
2. Fat embolism 
3. Air embolism 
4. Nitrogen embolism

 Emboli result in partial or complete vascular occlusion. 

 The consequences of thromboembolism include ischemic necrosis (infarction) of downstream tissue

PULMONARY THROMBOEMBOLISM
- 95% originate from deep veins of L.L

Special variants: - Saddle embolus: at bifurcation of Pulmonary artery

Paradoxical embolus: Passage of an embolus from venous to systemic circulation through IAD, IVD

CLINICAL CONSEQUENCE OF PULMONARY THROMBOEMBOLISM :

Most pulmonary emboli (60% to 80%) are clinically silent because they are small 

a. Organization: 60 – 80 % 
b. Sudden death, Right ventricle failure, CV collapse when more than 60 % of pulmonary vessels are obstructed. 
c. Pulmonary hemorrhage: obstruction of medium sized arteries. 
d. Pulmonary Hypertension and right ventricular failure due to multiple emboli over a long time.

Systemic thromboembolism

Emboli traveling within the arterial circulation 
80% due to intracardiac mural thrombi
2/3  Lt. ventricular failure

 The major targets are: 
 
 1. Lower limbs 75% 
 2. Brain 10% 
 3. Intestines 
 4. Kidneys 
 5. Spleen

Fat embolism 

Causes 
1. Skeletal injury (fractures of long bones ) 
2. Adipose tissue Injury

Mechanical obstruction is exacerbated by free fatty acid release from the fat globules, causing local toxic injury to endothelium. - In skeletal injury, fat embolism occurs in 90% of cases, but only 10% or less have clinical findings

 Fat embolism syndrome is characterized by 
 
 A. Pulmonary Insufficiency 
 B. Neurologic symptoms 
 C. Anemia 
 D. Thrombocytopenia 
 E. Death in 10% of the case 
 
 Symptoms appears 1-3 days after injury
 
 Tachypnea, Dyspnea, Tachycardia and Neurological symptoms
 
Air Embolism 

causes: 1. Obstetric procedures 
2. Chest wall injury 
3. Decompression sickness: in Scuba and deep-sea divers ((nitrogen )) 

 More then 100ml of air is required to produce clinical effect. 
 
 Clinical consequence
 1. Painful joints: due to rapid formation of gas bubbles within Sk. Muscles and supporting tissues. 
 2. Focal ischemia in brain and heart 
 3. Lung edema, Hemorrhage, atelectasis, emphysema, which all lead to Respiratory distress. (chokes) 
 4. caisson disease: gas emboli in the bones leads to multiple foci of ischemic necrosis, usually the heads of the femurs, tibias, and humeri
 
 Amniotic fluid embolism 
 - Mortality Rate = 20%-40% 
 - Very rare complication of labor 
 
 - due to infusion of amniotic fluid into maternal circulation via tears in placental membranes and rupture of uterine veins. 
 - sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures, DIC and coma 
 
 - Findings: Squamous cells, languo hair, fat, mucin …..etc within the pulmonary microcirculation