Nitric acid is commonly used in various industries. Its accidental spillage generates oxides of nitrogen, in­cluding N20, a potent pneumotoxin when inhaled. While the clinical presentation varies, a familiar feature is a period of relative well-being lasting a few hours, followed by rapidly progressive and often fatal, noncardiogenic pulmonary edema. Although its pathogenesis is not fully character­ized, the edema is a consequence of increased microvascular permeability, initiated by N02-mediated capillary injury. We report here findings in the lungs of three previously healthy young men who died of acute respiratory failure less than 24 h after an accident in a rural pulp-mill. The possibility that neutrophils and serum-derived mediators might play a role in the progression of the edema is raised by those findings.

Table 1—Some Clinical and Laboratory Data after Admission to Hospital

Clinical and
Laboratory Data

Patient
1

Patient
2

Patient
3

Age

36

44

21

Hospital
Admission

+9Vih

+ 9Vi h

+ 7У4

Feature on
admission

Respiratory rate

28

28

60

Blood pressure

180/100

86/0

130/80

Pulse

150

168

100

Arterial blood

+
9V£ h

-h
? 11
h

+
9V4h

+ 18Уа
h

+ 8
h

+ ? 9
h

pH

7.31

7.05

7.28

7.18

7.29

Pco,

30

71

29

74

45

53

Po,

50

37

45

46

43

58

HC03

15

19

17

26

25

Base Excess

-10

-15

-6

-5

-25

Chest
radiographs

Diffuse alveolar
pattern

Diffuse alveolar
pattern

Pulmonary edema

Hemoglobin
(g/lOQ

ml)

21.4

19.7

Hematocrit
(%)

64.3

58.6

White blood cell
count

30.4

22.9 (31.5
at
+ 14 h)

(1000/cm)

Segmented
(%)

65

77

Bands
(%)

22

11

Lymphocytes
(%)

10

4

Monocytes
(%)

3

8

Time of death

+ 13
h

+ 20
h

+ 21
h

Necropsy lung
weight (kg)

2.5

3.8

2.1

Case Reports

Occurrence

The men were exposed to fumes resulting from an explosion of a tank that contained approximately 1,736 L of 68 percent nitric acid. Investigations suggested that a valve controlling a connection between the tank and a pulp liquor line may have been left open and allowed the liquor to enter the tank, causing the explosion. The three men accidentally crossed over to the explosion area, where the dust and fumes were apparently heaviest. It took them approx­imately 10 to 15 min to escape from the building. No significant respiratory complaints or problems were apparent during examinations at a local clinic. However, increasing respiratory difficulties developed approximately 4 to 6 h later and they were rushed to a referral hospital, approximately 300 km away. One patient rapidly deteriorated in transit, however, and was taken to a regional hospital 130 km from the accident site. On admission, all were cyanotic with frothy fluid escaping from the nose and mouth. Mechanical venti­lation with PEEP was immediately instituted with rapidly progres­sive increments in the FIot to 100 percent. Other recorded salient features are summarized in Ibble 1 where the times after the accident are shown as “+ hours.” All died in less than 24 h. Viagra Online Canadian Pharmacy

Figure 1. LUng alveoli

Figure 1. Lung alveoli. Dark areas represent alveolar filling by proteinaceous edema fluid. This change is prominent around bronchioles (arrows) (hematoxvlin-eosin, original magnification x 115).

Necropsy Findings

The lungs were firm, up to five times heavier than normal (Table 1) and released abundant frothy fluid from all lobes. All showed bronchiolar epithelial necrosis, marked capillary engorgement and slight interstitial edema of alveoli. Notably, protein-rich edema fluid filled all alveolar spaces, most marked in peribronchiolar and, especially, alveolar duct areas (Fig 1) where thin hyaline membranes were also evident.

Figure 2. Lung alveoli after immunohistochemical

FIGURE 2. Lung alveoli after immunohistochemical staining for IgM with goat anti-human IgM antibody. The dark areas are deposits of IgM seen as linear “hyaline membranes” on alveolar epithelial surfaces and, in foci, within the interstitium [arrow) (original magnification x 2,500).

By immunohistochemistry studies, the protein-rich edema fluid contained albumin, fibrinogen and immunoglobulins G and M. IgM and fibrinogen also were found in the alveolar interstitium and in hyaline membranes (Fig 2). Electron microscopy of formalin-fixed lung revealed suboptimal technical preservation of structure. In better preserved areas degranulated and necrotic neutrophils were consistently found within alveolar capillaries, often spatially related to necrotic endothelial cells (Fig 3). Type 1 and 2 epithelial cells usually were absent or fragmented, probably due to artefacts.
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Figure 3. Electron micrograph of part of an alveolar

FIGURE 3. Electron micrograph of part of an alveolar capillary with its lumen filled by a degranulating necrotic neutrophil with a pyknotic nucleus (N). It is in contact with a necrotic endothelial cell (E). The alveolar surface of the wall is covered by poorly preserved cytoplasm of a type 1 epithelial cell {arrow) (original magnifica¬tion x 15,000).

Category: Diseases / Tags: Pulmonary Edema

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