What does a drowned body look like after 2 days

Unfortunately unattended deaths are common. As it becomes the norm for older generations to continue living on their own, and multigenerational households continue to not be the common tradition in America, people can pass without being discovered for some time.

We’re not going to post pictures of dead bodies. It’s disrespectful to the families and antithetical to what we do here at The BIOClean Team. But we can explain what decomposition does to bodies and what they might look like after 2 weeks, a month, and beyond.

First, there are four stages of decomposition

Autolysis, bloat, decay, and skeletonization. It begins immediately after death, about 4 minutes.

Autolysis is when the body begins to break down as blood stops circulating and breathing stops. When those two functions cease the body no longer has a way to remove waste such as carbon dioxide. That excess carbon dioxide creates an acidic environment that breaks down the cells, destroying them from the inside out.

Bloat follows. Autolysis will cause enzymes to leak out and then start to produce gases. During this stage, the body can double in size. Putrefaction begins here and usually is what alerts others to the death. It can linger long after the body has been removed.

The third stage is active decay. This is when the tissues, organs, muscles, and skin liquefy. The body loses the most mass during this stage.

Skeletonization is the final stage and it doesn’t have any set time frame.

What Does a Dead Body Look Like Immediately After Death?

Immediately after death, a body will look no different. There will be some mess, but the body itself will look mostly contained. As the first few days begin to pass the tissues will begin to decompose and the body will start to bloat. Foam might be present at the mouth and nose.

What Does a Dead Body Look Like After Two Weeks?

After two weeks the body will be bloated from gas. It will also appear red-colored as the blood decomposes.

What Does a Dead Body Look Like After Four Weeks?

After four weeks the body has begun to liquefy, with everything breaking down. Nails and teeth fall out.

What Does a Dead Body Look Like Beyond That? 

Much longer after a month, the remains of the body will be the skeleton and dark sludge of the liquified remains.

If a body is left unattended for this long in a home or vehicle, the work needed to be done to repair it is extensive. It’s far past cleaning, the space needs professional restorative work to create not just a clean space but a habitable one. 

Need help making a space livable again? Call the professionals at The BIOClean Team. We’re available 24/7 and offer caring, discreet services.

Call BIOClean Today!

After the storm (Slinkachu via the Telegraph)

(a) Evidence of drowning

Regardless of the composition of water/ fluid, ‘drowning’ (the ‘process of experiencing respiratory impairment from submersion in a liquid’ (van Beeck et al 2005)), may result in pulmonary surfactant insufficiency/ damage, pulmonary oedema, alveolitis, hypoxaemia, and metabolic acidosis (Modell 1993, Pearn 1985, Orlowski 1987).

Extensive experimental (animal) and clinical (human) data exist in the scientific literature, identifying differences between, for example, fresh water and seawater drowning; active respiration of fresh water results in alveolar collapse/ atelectasis, due to the alteration of the surface tension properties of pulmonary surfactant, resulting in intra-pulmonary shunts. Because it is hypotonic with respect to plasma, fresh water is rapidly absorbed into the bloodstream, causing transient (but clinically irrelevant) electrolyte dilution and hypervolaemia. Sea water causes surfactant loss, and because it is hypertonic with respect to plasma, results in fluid shifts into alveoli, plasma electrolyte hyperconcentration and hypovolaemia. (Modell 1993, Pearn 1985, Modell and Davis 1969, Modell et al 1966).

Fresh/ seawater aspiration leads to systemic hypoxaemia causing myocardial depression, reflex pulmonary vasoconstriction and altered pulmonary capillary permeability contributing to pulmonary oedema (Lunetta and Modell 2005).

Experimental evidence (Modell and Moya 1966, Modell et al 1967) shows that there is an inverse relationship between survival and the volume of aspirated fluid (sea water being twice as lethal as fresh water), but even small quantities (i.e. as little as 30 mL) caused arterial hypoxaemia.

Autopsy findings ascribed to drowning (‘external’ foam (i.e. visible at the mouth or nostrils), frothy fluid in the airways and lung ‘hyper-expansion’ reflect the pathophysiology of submersion and aspiration of the drowning medium; none of these, however, is diagnostic of drowning or present in all ‘verified’ drownings. (Lunetta and Modell 2005, Saukko and Knight (2004), Modell et al 1999).

In a series of 1590 bodies recovered from water, Lunetta et al (2002) found external foam in 29%, froth in the airways in 70.6% and overlapping of the lung margins in 64.1% of ‘fresh bodies’ of ‘verified drownings’; the combination of all three was present in only 8.8% of cases, but was said to be ‘100% specific for drowning’.

Suggested ‘signs of drowning’ reported in the literature include;

(i) External foam/ froth and frothy fluid in the airways reflects an admixture of bronchial secretion/ mucus, proteinacious material and pulmonary surfactant with the aspirated liquid (Lunetta et al 2002), which may persist for several days after death, and has been described as being ‘different in quality’ – more tenacious and persistent - from pulmonary oedema produced by other conditions (including cardiac failure, for example)(Modell et al 1999). Frothy secretions may be ‘washed away’ by flowing water during the submersion or recovery period, or may be absent due to the length of time spent immersed.

(ii) ‘Emphysema aquosum’ is the term used to describe hyperexpanded and ‘waterlogged’ lungs, whose medial margins ‘meet in the midline’, and which do not collapse on removal from the body. There may be ‘rib imprints’ on their pleural surfaces, and copious frothy fluid may exude from their cut surfaces (Giertsen 2000, Saukko and Knight 2004). See Magdeburg University's Virtual Pathology website for a 'pot specimen' of emphysema aquosum whichwhich can be rotated using your mouse wheel.

Combined lung weight of over 1Kg are comparable with ‘normal’ lung weights (de la Grandmaison et al 2001), but overlapping with that seen in fresh water drownings in Copeland’s series (Copeland 1985). However, Lunetta et al (2002) argue that lung weight alone is of ‘limited value’ for the diagnosis of drowning.

(iii) Pleural fluid accumulation. It has been stated (Morild 1995) that there is an association between drowning, post mortem submersion/ immersion interval and pleural fluid accumulation. However, data to the contrary has been presented by Yorulmaz et al (2003).

(iv) Sub-pleural haemorrhages (‘Paultauf’s spots’). These probably reflect haemolysis within intra-alveolar haemorrhages, and have been described in 5-60% of drownings (Lunetta and Modell 2005).

(v) Additional (morphological) ‘signs’ of drowning - ‘middle ear congestion and haemorrhage’, bloody/watery fluid in the sinuses and engorgement of solid organs, including the liver, reduction in the weight of the spleen, and muscular haemorrhages in the neck and back, are non-specific (Lunetta and Modell 2005).

(vi) Microscopy (particularly of the lungs) in the diagnosis of drowning has been described as yielding ‘nothing conclusive’(Giertsen 2000) and is ‘unreliable’ (Saukko and Knight 2004); there may be distension and/ or rupture of alveolar walls, alveolar haemorrhage and ‘narrowing of pulmonary capillaries’ (Lunetta and Modell 2005).

(vii) Diatom testing. Samples of major organs, and bone marrow, are often retained for diatom testing (eg. Kidney, liver, brain). The utility of such testing is ‘controversial’ (Peabody 1980); diatoms have been said to be ubiquitous in food and the environment, in non-drowning deaths, and absent in ‘known cases of drowning’. (Saukko and Knight 2004, Hendy 1973, Foged 1983).

(viii) Blood chloride content/ specific gravity analysis is considered to be ‘of no practical utility for the diagnosis (of drowning)’ (Lunetta and Modell 2005); analysis of blood strontium (Azaparren et al 1998) has also been suggested as a means with which drowning may be diagnosed.

Diatoms under the microscope

Source: Suspicious anatomy

(b) Evidence of an alternative mechanism(s)?

Drowning without evidence of liquid aspiration (‘dry drowning’) has been reported in up to 15% of cases, although in a series of 578 adults presumed to have drowned (Lunetta et al 2004), only 1.4% had lungs of ‘normal weight’ and no macroscopic signs of over-inflation.

Rather than represent true ‘drowning’, these deaths may be due to an alternative mechanism such as trauma, the effects of intoxication, arrhythmia, laryngospasm, or some other neurologically mediated mechanism (Modell et al 1999, Saukko and Knight 2004).

Stimulation of trigeminal nerve receptors by immersing the face (and laryngeal/ pharyngeal mucosa) in water has been shown to elicit reflex apnoea, bradycardia and peripheral vasoconstriction in humans- the so-called ‘diving response’ (Suzuki 1996, De Burgh Daly et al 1979), which is augmented by anxiety/ fear (Wolf 1966), a water temperature of less than 20 ºC (Pearn 1985) and, possibly, alcohol (Pearn 1984), increasing the likelihood of the development of a fatal arrhythmia. Cardiac arrest has also been documented following entry of water into the nose (Datta and Tipton 2006).

The ‘cold shock response’ - initiated by peripheral subcutaneous receptors - causes respiratory effects (inspiratory gasp and uncontrolled hyperventilation, respiratory alkalosis, cerebral hypoxia and possibly ventricular fibrillation) and cardiovascular effects (tachycardia, increased cardiac output, hypertension and ‘heart strain’, potentially leading to cardiac irritability and ventricular fibrillation), which appear temperature dependent (Tipton 1989, Datta and Tipton 2006). Co-stimulation of both diving and cold shock responses may precipitate supraventricular arrhthmias (Golden et al 1997).