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Background Introduced in 1970, the Swan–Ganz catheter (SGC) soon became widely used because of its unique usefulness in managing intensive care patients. Unfortunately, SGC usage was complicated by pulmonary artery rupture (PAR) with a 50% mortality rate that led to a near banning of the SCG in the late 1980s. Increasing knowledge and decreasing incidence of SGC-related PARs (SGPARs) led to the current feeling that the present SGPAR incidence is now low enough to tolerate given the lives saved by SGC usage. However, an important unknown is that, to our knowledge, pathologists have never published a comprehensive microscopic description of a SGPAR. Case report A 73-year-old woman with moderate pulmonary hypertension died from a SGPAR soon after single SGC measurements of right ventricular and pulmonary capillary wedge pressures. By using what we thought to be an appropriate method of dissection, we did a complete microscopic step section study of the 1.6 cm SGPAR revealing 12 relatively uniform longitudinal tears (one perforating) consistent with an overinflated SGC balloon or a weakened arterial wall. Literature review A MEDLINE search of 38 consecutive SGPARs from 2014 to 1980 found 52 cases in 38 papers. Analysis revealed that all 46 SGPARs suitable for study came from large institutions, and confirmed that elderly women were more likely to have SGPARs than elderly men. Conclusions More and better data are needed before fully informed decisions can be made regarding future SGC usage.

The development of extra efferent vessels (EEV) is a little-known feature of diabetic glomerulopathy. The only previous large study [Min W, Yamanaka N. Three-dimensional analysis of increased vasculature around the glomerular vascular pole in diabetic nephropathy. Virchows Archiv A Pathol Anat 1993; 423:201-7] known to us found that up to 5 EEV per glomerulus (glom) each drained a separate lobule. Most EEV connected to the second- and third-order branches of the afferent arteriole (AA), and drained into peritubular capillaries. Although not so stated, the illustrations suggested that some EEV could be shunts, and thus detrimental to glom function, and possibly glom health. There was no correlation between the unquantitated presence of increased EEV at the vascular pole (VP) and the severity of the major diabetic glomerular (glom) lesions. The authors opined that efferent arteriole (EA) stenosis by insudative lesions (IL) stimulated the formation of EEV. To confirm and extend these findings, we have repeated the study in 18 diabetic cases with mild to severe, but not end-stage, diffuse and nodular lesions (DL and NL), 8 controls, and the 2 normal traumatic nephrectomy cases. Up to 18 EEV per glom were found in diabetic cases along with occasional EEV in controls. EEV contained muscle and were almost identical to the EA in structure. Nearly all EEV connected with efferent glom capillaries at the VP, where they exited the glom through apparently preexisting gaps in the Bowman's capsule and/or glomerular capillary basement membranes (BCBM/GCBM). The EA exited through a similar gap, so the exit of EEV was accomplished without altering the anatomical relationships between the exiting vessels and the components of the VP thought to be important in the control of glom outflow. The largest number of EEV occurred in long-standing T2DM cases with mild to moderate DL and NL. Complete photographic glom reconstructions revealed numerous anastomoses among efferent glom capillaries in normal and diabetic gloms with mild to moderate DL and NL. No disproportionately dilated EEV were seen. The findings just cited confirm that EEV are common and surprisingly numerous in diabetic gloms. They suggest that EEV formation served to preserve glom function, and that EEV could neither shunt nor restrict glom outflow locally. In our opinion, the formation of EEV represents a significant, possibly hemodynamically induced, remodeling of the glom that should be added to the list of changes that occur in diabetes. It is hypothesized that EEV develop because of increased glom inflow, and that the latter may be attributable to AA muscle damage that impairs its contractile ability.

Kidneys from 74 consecutive, primarily non-insulin-dependent diabetics at autopsy and 59 age-, sex, and ethnic group-matched controls were examined qualitatively and semiquantitatively to determine the prevalence and severity of insudative lesions (ILs) and obsolescent glomeruli with (OGcFC) and without (OGsFC) insudative (fibrin cap) lesions. A subset of 25 cases with advanced diabetic changes was examined using serial sections, immunohistochemical stains, and electron microscopy to determine the pathogenesis of ILs and OGcFCs. Insudative lesions consisted of intramural accumulations (hereafter called deposits) of presumably imbibed plasma proteins and lipids within renal arterioles, glomerular capillaries, Bowman's capsule, and proximal convoluted tubules. Insudative lesions in Bowman's capsule are called capsular drop lesions (CDs), in glomerular capillaries they are called fibrin cap lesions (FC), and in afferent and efferent arterioles they are called hyalinized afferent (HA) and hyalinized efferent (HE) arterioles, respectively. All ILs were much more numerous and/or larger in diabetics than in controls. Contrary to previous opinion, CDs and HE arterioles were not specific for diabetes, being present in small numbers in nine (15%) controls. Controls with CD/HE arterioles had far more HA arterioles and focal mesangiolyses (FMs) than those without. Insudative lesions consisted of the well known homogenous eosinophilic deposits (homogenous eosinophilic ILs) and the less familiar foamy, reticulated, and vacuolar deposits (heterogenous lucent ILs). Homogenous eosinophilic ILs were predominant in afferent arterioles and more so in efferent arterioles, and were segregated into globules of varying density with the denser deposits located peripherally. Two types of CDs, which differed sharply in location and composition, were found. The first was mostly homogenous eosinophilic, usually without capsular adhesions and located near the vascular pole close to preglomerular arterioles. The second was mostly heterogenous lucent, located away from the vascular pole, and consistently connected by adhesions to the capillary tuft usually near FMs and/or Kimmelstiel-Wilson (KW) nodules. The latter ILs sometimes extended in continuity along the internal surface of the basement membrane from Bowman's capsule into the proximal convoluted tubule. It was hypothesized that ILs traveled centrifugally through the walls of preglomerular arterioles to form the first type of CD and longitudinally within the walls of afferent arterioles and glomerular capillaries and through adhesions to form the second. Contrary to previous opinion, FCs were consistently intramural. When numerous, FCs were associated with a form of glomerular obsolescence called OGcFC.(ABSTRACT TRUNCATED AT 400 WORDS)

Kidneys from 74 consecutively autopsied primarily non-insulin-dependent diabetes cases and 59 age-, sex-, and ethnic group-matched controls were examined qualitatively and semiquantitatively to determine whether focal mesangiolyses (FMs), Kimmelstiel-Wilson (KW) nodules, and glomerular capillary microaneurysms (GCMs) were related lesions, to determine their extent and pathogenic sequence, and to look for associations with structural and functional factors. Light microscopic examination of serial sections, immunohistochemical stains, image analysis, and electron microscopy were used. Focal mesangiolyses, KW nodules, and GCMs occurred in 31 of the 74 diabetes cases (27 had FMs, 29 had KW nodules, and nine had GCMs) and were positively correlated with each other semiquantitatively (r = .71, .70, and .68, respectively). Numerous FMs were found, involving 62% and 78% of the glomeruli in the two most severely affected cases. Most FMs were located at the periphery of KW nodules, but de novo FMs were documented in six cases. Glomerular capillary microaneurysms were deemed occasional complications of FMs because they were much less common, and 25 of the 27 GCMs identified were contiguous with FMs. Focal mesangiolyses and GCMs were deemed transient lesions, being absent in end-stage kidneys. Both FMs and KW nodules consisted of a spectrum of lesions. For the sake of clarity they were arbitrarily divided into two types: edematous and proliferative FMs and simple and complicated KW nodules. Their characteristics suggested the following pathogenic sequence: edematous FM-->proliferative FM-->focal nodular mesangial expansion-->simple KW nodule-->recurrent FM-->complicated KW nodule. Complicated nodules were associated with marked alterations in the lobular capillary. The number of mesangial cells was increased in FMs and they were thought to be responsible for increased matrix production. Focal mesangiolyses and KW nodules were positively associated with diabetes, proteinuria, and hyalinization of afferent and efferent arterioles, but were weakly or not associated with hypertension, arcuate and interlobular artery stenosis, hydroenphrosis, acute pyelonephritis, renal arterial atheromatous emboli, glomerular platelet-fibrin thromboemboli, and congestive heart failure.

Lesions resembling diffuse intimal thickening (DIT) in morphology are reported in the left anterior descending coronary arteries and aortas of 2 1 2 - year-old miniature swine. The lesions are similar in composition and location to those previously described under a variety of names in swine, either large or miniature. The lesions are intermediate in size when compared with those of younger and older swine, and when all the data are seen together, a picture emerges of gradually enlarging musculoelastic lesions which eventually assume a double or triple-layered structure. The lesions are mostly focal, and are most pronounced in the abdominal aortas where their rather constant localization to proximal posterior and distal anterior walls suggests thay they are caused in part by hemodynamic stresses.

Hearts from 1,676 consecutive autopsies were examined over a 4 1/2 year period between 1980 and 1984. Forty-seven (4.3%) of 1,083 adult hearts were found to have from one to nine distinctive bulbous thickenings (BTs) involving the mitral valve chordae tendineae. By light- and electron-microscopy, the BTs were found to consist of numerous myofibroblasts, collagen, and elastin layered over otherwise normal chordae and occasionally involving adjacent valve leaflets. No evidence of inflammation, rheumatic or otherwise, was found in histologic sections of the mitral, aortic, and tricuspid valves, or in samples of myocardium from all chambers. No BT was present in 593 hearts from infants and children, indicating that the lesions were acquired. Review of autopsy diagnoses showed that 14 (29.8%) of the 47 patients with BT had alcoholic hepatitis or micronodular cirrhosis, as opposed to 80 (7.7%) of the 1,036 patients without BT. This difference was highly statistically significant (P less than 0.01). The prevalence of viral liver disease was similar in the two groups. Of all patients with alcoholic liver disease, those with BT tended to be male and older. BT appears to be a distinctive process that is strongly correlated with alcoholic liver disease.

In an epidemiologic study of Reye's syndrome in the state of Oklahoma over a 21 month period, a cluster of cases involving 11 patients, all of whom died, was identified. Eight of these cases occurred over a 4 month period and, on the basis of epidemiologic and laboratory evidence, appear to have been associated with a concurrent epidemic of influenza B virus infection.

The case of a patient with primary hyperparathyroidism in whom water-clear-cell hyperplasia (WCCH) involved only the superior glands, and disproportionately so, is presented. In addition, unlike the cases of WCCH described previously, a rim of normal parathyroid tissue was observed at the periphery of each gland in this case. It is speculated that these findings are not necessarily peculiar, but may reflect an earlier stage of the disease. Such cases may mimick parathyroid adenoma, thereby leading to inadequate surgical therapy.