Biomedical subjects
Publications and source records attributed to V Freudenberg.
A premature baby requiring mechanical respiratory aid because of severe IRDS developed an interstitial pulmonary emphysema and died of massive gas embolism. Air trapped in the pulmonary interstitium because of rupture of overinflated alveoli, penetrated into the pulmonary lymphatics and entered the venous system via the thoracic duct.
362 preterm newborns with birth weights ranging between 1 000 and 2 000 g were admitted to NICU of Kinderklinik Städtische Kliniken Kassel during Jan. 1978 and Dec. 1981. 160 babies (44%) needed breathing support (CNP, CPAP, IMV, IPPB). Pneumothorax occurred in 22 babies, 17 died. A severe cerebral hemorrhage was diagnosed in 12 (55%) of these babies on the basis of pathological and/or clinical findings. Cerebral hemorrhage followed pneumothorax. An air leakage syndrome was seen 15 times in 36 children with cerebral hemorrhage (42%). Pneumothorax causes not only intracranial hemodynamic changes, but also acute hypoxemia and slowly increasing hypercarbia, factors strongly contributory to cerebral hemorrhage in the premature baby. This point must be considered in the present discussion about high frequency ventilation for prevention of bronchopulmonary dysplasia. High frequency ventilation with presently traded ventilators is more correlated with alveolar rupture than low frequency ventilation.
A case with pneumopericardium and pneumomediastinum produced by a bronchial foreign body (pieces of a nut) is reported. The pathomechanism is discussed: In state of check valve the bronchial foreign body produces an interstitial emphysema by rupture of the alveolar membranes in the overinflated lung. The interstitial air travels along the sheaths of the pulmonary blood vessels to the root of the lung, to mediastinum, and to pericardium. In state of stop valve, depending on the inflammatory swelling of the mucosa, the affected lung becomes atelectatic. After removing the foreign body air passage will be free. Other therapeutic measures are not necessary.
This is a case-report about a 4 year old boy with "cherry red" epiglottis, purulent meningitis and pleuropneumonia. Purulent meningitis and pleuropneumonia are not complications of treatment of "cherry red" epiglottis but an entity caused by Hemophilus influenzae-infection and is called Kleinschmidt's syndrome (Hemophilus influenzae type B-infection-syndrome). This severe illness is successfully treated if recognized early enough. At present, chloramphenicol is the therapy of choice. Intubation or tracheotomy are important but supportive measures.
13 unselected premature infants with idiopathic respiratory distress syndrome (IRDS) have been treated with continuous negative pressure (CNP). A chamber was applied to the infants' body, so that the head remained outside in normal atmospheric pressure. 4 infants died during the period of treatment. 6 out of 13 differently treated IRDS-infants died over the same 6 months period. In comparison 18 out of 27 infants with IRDS died the previous year, during the same period. The frequency of IRDS in both observation periods was the same, as was the therapy of acidosis and hypoxia. The infants responded to CNP with decreased respiratory frequency, lessening of "grunting" and return of a pink skin color. Pathological examination of 3 out of 4 deceased infants in the study group revealed both atelectases and some degree of interstitial emphysema and widened capillaries. No intravascular hyaline thrombi were seen. The remaining infant died with clinical signs of coagulopathy (no autopsy). Of the 9 surviving infants in the study group one developed a hydrocephalus and subsequent mild psychomotor developmental retardation. We conclude that the CNP therapy in the chamber is an asset to the treatment of early and medium-severe cases of IRDS. We believe, that early application might prevent development of severe IRDS. The method is not recommended for severe cases.
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A newborn baby was born with scrotal hematoma and a diagnosis of testicular torsion was made. This diagnosis proved false, when the hematoma was resorbed after a few days and other hematomas developed instead (abdomen, elbow, foot, scalp). A total of nine hemorrhagic episodes were observed, most of them occurring on the scalp. All lesions were sharply delineated, started with red to purple discoloration and then turned to bluish-black indicating gangrene. Histology revealed extensive bleeding into the corium, fibrin thrombi within the capillaries, and complement and IgG in the small arterial walls. Each bleeding was associated with hypofibrinogenemia and thrombocytopenia. A diagnosis of hereditary protein C deficiency was made. Blood levels were consistent with heterozygosity of both the parents and homozygosity of the child. Bleedings were controlled by Cohn fraction I and heparin. It was impossible, however, to prevent further hemorrhage by continuous i.v. heparin. In addition aprotinin, epsilon-aminocaproic acid, AT III, and prednisone were ineffective. Continuous remission finally could be sustained with oral phenprocoumon.