Latent oedema

Disorders of cerebral functions on the one hand and of the water and electrolyte balance on the other hand are the earliest and most reliable hints of the onset of decompensation in severe liver disease, especially cirrhosis. In clinical terms, they can be easily diagnosed as latent hepatic encephalopathy (by carrying out psychometric tests) and/or latent oedema (by recording the increase in body weight). For this reason, these examination methods are also of fundamental importance in the follow-up of chronic liver disease, (s. fig. 15.3)... 

Patients should immediately consult the doctor if their body weight rises steadily by > 1 kg over a period of 3 or 4 days. This is suggestive of a clinically not yet identifiable accumulation of water in the tissue (= latent oedema). Patients should also consult the doctor in the case of minor irregularities in their handwriting. Psychometric tests can be used to confirm or discount suspected cases of latent HE. (s. pp 203, 272) (s. fig. 15.3)... 

The development of latent oedema can be recognized by means of daily weight checks when an increase in weight of > 1 kg occurs within 4 days. 

Impairment of cerebral functions and disturbances of the water and electrolyte balance are the two most important and most common manifestations of decompensated liver cirrhosis. They may be reliably detected at an early stage by means of daily body weight control and simple psychometric tests. A documentation sheet filled in by the patient has proved to be worthwhile latent oedemas or the onset of ascites as well as latent encephalopathy can be detected in this way and thus treated at an early stage. Longterm standing leads to a reduction of natriuresis with subsequent water retention and a deterioration of renal blood flow (like a vicious circle). This is caused by activation of the RAAS and the sympathetic nervous system. Such a dangerous situation (which can arise for example after two hours of standing at a sports event with excessive emotional participation) is often underrated, as we ourselves observed in several patients (s. p. 292) (s. fig. 15.3) (see chapter 16 )... 

Ascites The oeeurrence of a disturbed water-eleetrolyte balance in the late stage of latent oedema (s. fig. 15.3) (s. p. 297) requires immediate restriction of the salt intake (<3-6 g/day) - depending on the level of natriuresis the intake of fluid is limited to 1.0 (-1.5) 1/day especially in hyponatriaemia. An intermittent fruit and rice diet (generally for 1-2 days) is recommended because it is extremely low in sodium, but rich in potassium. Marked NaCl restriction simultaneously leads to a reduction in protein intake. The use of commercially available low-salt protein preparations is therefore advisable (e.g. 60 g protein/100 g + 5 mval sodium/100 g, or 48 g protein/100 g + 13 g, or 15 g sodium/100 g). 

Diagnosis is determined on the basis of anamnesis about gas contact with specific smell (in gas mixtures it may not be established), about the combination of a latent period of specific duration after catarrhal phenomena with pulmonary oedema. 

The inhalation of phosgene in toxic quantities produces pulmonary oedema. The exact mechanisms involved remain remarkably obscure in particular, the latent period, see below, is puzzling. No discussion of the effects of phosgene can be undertaken without a careful examination of current concepts of tissue fluid balance. These have changed substantially since WWI, although the early work of Starling (1896) has largely stood the test of time. 

Toxic symptoms initially slight ocular and bronchial irritation, lachrymation, nausea after a latent period of about 6 to 16 hours, feeling of sickness, restlessness, shortness of breath, and pulmonary oedema. 

Diller describes three main phases associated with phosgene induced lung injury as the initial reflex syndrome, the clinical latent phase and the clinical oedema phase. ... 

Following a variable latent period ranging from 1 to 24 h, there may be signs of developing pulmonary oedema with dyspnoea, coughing and the production of large amounts of foamy sputum (Fig. 7.2). 

Fig. 7.2 A field hospital during the First World War. Casualties with toxic pulmonary oedema following a gas attaek outside a field hospital during the First World War. Little could be done for such cases, apart from providing bed rest during the latent period of possible development of pulmonary oedema following the exposure. (Source The National Archive)...

Proactive to mitigate and pre-empt developing type 1 respiratory failure with the development of toxic pulmonary oedema and acute respiratory distress syndrome during a latent period following exposure. 

---